Mitochondria: The Powerhouse of the Cell Explained

I. Introduction

Mitochondria have long been dubbed the powerhouse of the cell, a phrase that encapsulates their crucial role in energy production through the process of oxidative phosphorylation. These double-membrane organelles not only generate adenosine triphosphate (ATP), the primary energy currency of the cell, but also engage in various other vital functions, including the regulation of metabolic pathways and apoptosis. Understanding mitochondria extends beyond their energetic contributions, delving into their implications in cellular health and the etiology of numerous diseases, such as diabetes and neurodegenerative disorders. This essay seeks to unravel the complex nature of mitochondria, addressing their structure, function, and significance in cellular physiology. By critically analyzing recent research on mitochondrial dynamics and their impact on cellular homeostasis, we can appreciate the intricate connections between mitochondrial function and overall organismal health, establishing a foundation for potential therapeutic interventions.

A. Definition and significance of mitochondria

Mitochondria are double-membraned organelles often referred to as the “powerhouses of the cell” due to their crucial role in adenosine triphosphate (ATP) production through oxidative phosphorylation. Located primarily in eukaryotic cells, these organelles not only generate energy but also participate in vital metabolic pathways, including the Krebs cycle, which is central to energy production. Beyond energy metabolism, mitochondria are implicated in diverse cellular processes such as apoptosis, calcium signaling, and reactive oxygen species (ROS) management, highlighting their significance in maintaining cellular homeostasis. For instance, the Arabidopsis thaliana COX11 protein demonstrates the critical involvement of mitochondria in energy production and copper homeostasis. Disruptions to COX11 expression lead to severe physiological consequences, including inhibited root growth and impaired reproductive processes, underscoring mitochondrial importance in plant vitality and function (Mansilla et al.). Ultimately, the multifaceted roles of mitochondria extend beyond mere energy production, making them indispensable to both cellular health and organismal development.

B. Overview of mitochondrial functions

Mitochondria are fundamental organelles in eukaryotic cells, primarily recognized for their role in adenosine triphosphate (ATP) production through oxidative phosphorylation. This essential function allows mitochondria to serve as the energy currency of the cell, facilitating various cellular processes, including biosynthesis, cell signaling, and regulation of metabolic pathways. Beyond energy production, mitochondria also play a crucial role in maintaining cellular homeostasis through apoptosis and the modulation of reactive oxygen species (ROS). Recent studies highlight the importance of uncoupling proteins, particularly uncoupling protein 2 (UCP2), which helps mitigate oxidative stress by reducing mitochondrial membrane potential and dissipating excess metabolic energy (Forte et al.). Moreover, emerging insights into mitochondrial dysfunction link these organelles to various diseases, including vascular ailments and cancer, suggesting their potential as therapeutic targets for novel interventions (Jeena et al.). Thus, understanding mitochondrial functions is vital for illuminating their diverse roles in cell biology and disease pathology.

Function	Description	Significance	Current Statistics
ATP Production	Mitochondria generate adenosine triphosphate (ATP) through oxidative phosphorylation.	ATP serves as the primary energy currency of the cell.	Up to 95% of cellular ATP is produced by mitochondria.
Regulation of Metabolism	Mitochondria play a critical role in the metabolic process, including the Krebs cycle.	They help convert carbohydrates, fats, and proteins into usable energy.	Involved in the metabolism of multiple nutrients, contributing to over 70% of energy production.
Calcium Homeostasis	Mitochondria regulate calcium levels within cells.	Calcium signaling is crucial for various cellular processes, including muscle contraction and neurotransmitter release.	Mitochondria can uptake and release calcium ions, affecting cellular calcium levels by up to 40%.
Apoptosis Regulation	Mitochondria are involved in the intrinsic pathway of programmed cell death (apoptosis).	They release cytochrome c, which triggers caspases for the execution of apoptosis.	Mitochondrial dysfunction can lead to improper apoptosis, contributing to diseases like cancer and neurodegeneration.
Reactive Oxygen Species (ROS) Management	Mitochondria produce and manage reactive oxygen species as a byproduct of ATP production.	ROS play a role in cell signaling but can cause oxidative stress if not regulated.	Around 1-3% of oxygen consumed by mitochondria is converted to ROS.

Mitochondrial Functions Overview

C. Importance of studying mitochondria in cellular biology

The study of mitochondria is vital in cellular biology due to their integral role in energy production and their implication in various diseases. Mitochondria are not only essential for ATP synthesis through oxidative phosphorylation but also serve as key players in metabolic regulation and apoptosis. Recent research has highlighted that mitochondrial dysfunction can lead to a range of pathologies, including neurological disorders and metabolic syndromes. For instance, mitochondrial diseases have been associated with conditions such as epilepsy, autism, and even bipolar disorder, showcasing the mitochondrias influence beyond mere energy metabolism (Atchison et al.). Additionally, proteins such as PINK1, PARKIN, and DJ-1 have emerged as crucial components in mitochondrial quality control, revealing their potential roles in cancer biology as well (Lucas et al.). Consequently, understanding mitochondrial dynamics and pathology not only enriches our comprehension of cellular function but also opens avenues for therapeutic interventions in myriad diseases.

II. Structure of Mitochondria

The intricate structure of mitochondria is paramount to their function as the cells powerhouse. Comprised of the outer membrane, intermembrane space, inner membrane, and the matrix, each component plays a critical role in energy production and metabolic processes. The outer membrane, smooth and permeable, houses proteins that facilitate the transport of ions and small molecules, whereas the inner membrane is extensively folded into cristae, significantly increasing its surface area for ATP synthesis. This structural adaptation is crucial for the efficient functioning of the electron transport chain, where oxidative phosphorylation occurs ((Dang et al.)). Additionally, the matrix contains enzymes necessary for the Krebs cycle, which further underscores the organelles multifaceted role in cellular respiration. As researchers continue to analyze mitochondrial architecture, a deeper understanding emerges regarding its implications in health and disease, notably in conditions linked to mitochondrial dysfunction ((Dacks et al.)).

A. Description of mitochondrial membranes

The mitochondrial membranes play a pivotal role in maintaining cellular energy metabolism and regulating various biochemical processes. Composed of an inner and outer membrane, the structural configuration of these membranes is essential for their respective functions. The outer membrane, which is permeable to small molecules and ions, contains porins that facilitate the passage of metabolites essential for cellular respiration. In contrast, the inner membrane is highly invaginated into structures known as cristae, maximizing surface area for critical processes, such as oxidative phosphorylation and ATP synthesis. This membrane harbors numerous transport proteins and enzyme complexes that are vital for the electron transport chain. Moreover, alterations in mitochondrial membrane integrity can disrupt energy production and have been implicated in various pathologies, including neurodegenerative diseases. For instance, dysfunctional mitochondria from chronic ovarian hormone deprivation exhibit lipid profile changes, showcasing the membranes significance in cellular health (Alvarez et al.) and (Anderton et al.).

B. Role of mitochondrial DNA

Mitochondrial DNA (mtDNA) plays a critical role in the function and integrity of mitochondria, serving as a key component in cellular energy production and metabolic regulation. Unlike nuclear DNA, which encodes the majority of mitochondrial proteins, mtDNA is primarily responsible for encoding essential components of the electron transport chain and ATP synthesis, underscoring its vital influence on cellular bioenergetics (Jiang et al.). Additionally, the interplay between mtDNA and nuclear DNA is crucial for maintaining cellular homeostasis, particularly during stress responses. This communication facilitates adaptations in energy metabolism, which are necessary for processes such as cell cycle progression and cellular survival under adverse conditions. Furthermore, disruptions in mtDNA can lead to mitochondrial dysfunction and are implicated in various diseases, including heart failure and cancer, where cellular energy demands become unbalanced (Ganeshan K et al.). Thus, mtDNA serves not only as a genetic reservoir but also as an integral determinant of mitochondrial efficiency and overall cellular health.

C. Unique features of mitochondrial morphology

Mitochondria exhibit unique morphological characteristics that are pivotal to their functionality and adaptability within various cellular contexts. These organelles are not static; rather, they exhibit dynamic processes of fusion and fission, which enable them to adjust their shape and size in response to cellular stressors and metabolic demands. Such morphological plasticity is essential for maintaining mitochondrial integrity and optimizing energy production. For instance, during periods of oxidative stress or metabolic challenges, as highlighted in research involving neuroblastoma cells, the alteration of mitochondrial shape correlates with changes in protein expression implicated in energy metabolism ((Deighton et al.)). Furthermore, the distinct structures of mitochondria, including their inner and outer membranes, enhance their ability to regulate apoptotic pathways and ATP synthesis, reinforcing their central role as bioenergetic hubs in the cell ((Jeena et al.)). Ultimately, these unique features of mitochondrial morphology are fundamental to their role as the powerhouse of the cell.

III. Mitochondrial Function and Energy Production

Mitochondria are integral to cellular energy production, operating as bioenergetic hubs that generate adenosine triphosphate (ATP) through oxidative phosphorylation. This process is not merely a biochemical event; it influences various cellular functions, impacting overall cell health and viability. Notably, the protein leucine-rich-repeat kinase 2 (LRRK2) has emerged as a significant player in mitochondrial dynamics, particularly regarding energy production in immune cells. Elevated kinase activity associated with LRRK2 mutations has been linked to mitochondrial dysfunction, leading to impaired ATP synthesis, which can ultimately trigger cellular apoptosis. These findings indicate that mitochondrial efficiency is crucial in preventing the demise of neurons, particularly in neurodegenerative diseases like Parkinsons. Furthermore, as emerging studies suggest a connection between mitochondrial health and the inflammatory processes involved in the progression of such diseases, understanding LRRK2s role highlights the mitochondrias indispensable function in both energy production and cellular integrity (Oun et al.), (Haas et al.).

A. Overview of cellular respiration processes

Cellular respiration serves as a fundamental metabolic pathway, orchestrating the conversion of biochemical energy from nutrients into adenosine triphosphate (ATP), which is essential for various cellular functions. This complex process primarily occurs within mitochondria and can be categorized into three distinct stages: glycolysis, the citric acid cycle, and oxidative phosphorylation. Glycolysis takes place in the cytoplasm, where glucose is broken down into pyruvate, generating a modest yield of ATP and NADH. Subsequently, pyruvate enters the mitochondria, fueling the citric acid cycle, which produces additional electron carriers, NADH and FADH2, crucial for the next phase. The final stage, oxidative phosphorylation, utilizes these electron carriers to facilitate ATP production through the electron transport chain, a process tightly linked to mitochondrial dynamics, as ATP synthesis efficiency is influenced by changes in mitochondrial morphology. Hence, understanding these processes illuminates the pivotal role of mitochondria in bioenergetics and cellular functionality.

B. ATP synthesis and the electron transport chain

The synthesis of adenosine triphosphate (ATP) occurs predominantly through the intricate processes of the electron transport chain (ETC), located within the inner mitochondrial membrane. This chain comprises a series of protein complexes that facilitate electron transfer from NADH and FADH2, ultimately culminating in the reduction of oxygen to water. As electrons traverse the ETC, energy released is harnessed to pump protons into the intermembrane space, establishing an electrochemical gradient. This proton motive force drives ATP synthesis via ATP synthase, where protons flow back into the matrix, catalyzing the conversion of adenosine diphosphate to ATP. Notably, disruptions in mitochondrial function, such as those affecting the ETC, can severely impair ATP production, as demonstrated by the detrimental effects of certain compounds like verrucosidin, which inhibit complex I and hinder energy production under glucose deprivation. Such insights underscore the dependence of cellular energetics on mitochondrial integrity and function ((Abdul et al.)).

The chart illustrates the relationship between ATP synthesis processes and the impact of mitochondrial function disruptions. It highlights the number of key components involved in the Electron Transport Chain alongside the level of impact on cellular energetics caused by the compound Verrucosidin. The blue bar represents the total number of key components, while the red bar indicates the severity of the impact, measured on a scale from one to five. This visualization emphasizes the dependence of ATP production on mitochondrial integrity and function.

C. Role of mitochondria in metabolic pathways

Central to the functionality of mitochondria is their pivotal role in metabolic pathways that sustain cellular energy homeostasis. These organelles not only generate adenosine triphosphate (ATP) through oxidative phosphorylation, but they also play a crucial part in biosynthetic processes by supplying metabolic intermediates essential for macromolecule synthesis and post-translational modifications. Recent studies underscore the dynamic interplay between mitochondrial morphology—shaped by the balance of fusion and fission events—and metabolic activity, revealing how metabolic signals can modulate mitochondrial structure and function to meet cellular demands. When faced with energy supply-demand mismatches, such as during hypoxia, mitochondrial adaptation mechanisms are activated, contributing to metabolic modulation and optimizing oxygen utilization. Thus, the intricate connectivity between mitochondrial dynamics and metabolic pathways underscores their foundational role in maintaining cellular energy balance and responding effectively to physiological challenges.

The chart presents the roles of metabolic pathways in mitochondrial function, highlighting five key categories: ATP Generation, Biosynthetic Processes, Fusion and Fission Dynamics, Hypoxia Response, and Mitochondrial Health. Each category is assigned a significance level, illustrating the importance of each role in maintaining mitochondrial function and energy homeostasis. The visual is designed to effectively communicate the relative contributions of these pathways to the overall cellular energy dynamics.

IV. Mitochondria and Cellular Health

Mitochondria are pivotal in maintaining cellular health through their roles in energy production and metabolic regulation. They function as the primary energy generators in eukaryotic cells, converting nutrients into adenosine triphosphate (ATP), which is essential for cellular processes. However, mitochondrial dysfunction can lead to a cascade of health issues, including obesity and metabolic disorders, as observed in studies highlighting their role in energy homeostasis (Guo et al., 2016). This dysfunction can result from inadequate ATP production, oxidative stress, and inflammation, ultimately disrupting cellular equilibrium. Furthermore, dietary factors significantly influence mitochondrial performance, underscoring the intricate connection between nutrition and cellular health ((Sarmidi et al.)). By addressing mitochondrial efficiency through targeted nutritional strategies, it may be possible to enhance metabolic balance and prevent disease. Thus, understanding mitochondrial dynamics is crucial for developing interventions that promote overall cellular vitality and metabolic stability.

A. Impact of mitochondrial dysfunction on diseases

Mitochondrial dysfunction is increasingly recognized as a pivotal factor in the pathogenesis of various diseases, particularly neurodegenerative disorders like Alzheimer’s disease. This impairment in mitochondrial function disrupts ATP production and leads to an imbalance in cellular homeostasis, which can initiate neurodegenerative processes through oxidative stress and inflammation. Research has shown that impaired energy metabolism in neurons significantly contributes to the vulnerability observed in these conditions, with proteomic studies revealing extensive alterations in protein expression linked to mitochondrial energy production and cellular stress responses ((Deighton et al.)). Moreover, the dynamic morphology of mitochondria—shaped by fission and fusion events—plays a critical role in modulating metabolic functions essential for processes such as immune response and cell survival. Therefore, understanding the mechanisms underlying mitochondrial dysfunction is crucial for developing therapeutic strategies aimed at alleviating the burden of diseases linked to these vital organelles.

Disease	Mitochondrial Dysfunction Role	Prevalence (% of Population)	Key Findings
Alzheimer’s Disease	Reduced ATP production and increased oxidative stress	6.7	Mitochondrial deficits are linked to neurodegeneration.
Parkinson’s Disease	Impairment of complex I in the electron transport chain	1	Mitochondrial dysfunction contributes to dopaminergic neuron death.
Diabetes Mellitus	Altered fatty acid oxidation and insulin resistance	10.5	Mitochondrial dysfunction is associated with metabolic dysregulation.
Cardiovascular Diseases	Impaired oxidative metabolism leading to heart failure	6.2	Mitochondrial defects can exacerbate heart conditions.
Charcot-Marie-Tooth Disease	Impaired axonal transport affecting neuronal health	0.01	Mitochondrial dysfunction recognized in hereditary neuropathies.

Impact of Mitochondrial Dysfunction on Diseases

B. Mitochondrial biogenesis and its regulation

Mitochondrial biogenesis, defined as the process through which new mitochondria are formed within cells, is intricately regulated by a network of signaling pathways responding to cellular energy demands and stressors. This regulation is crucial because the biogenesis of mitochondria ensures that their numbers and function align with cellular requirements, particularly in tissues with high energy consumption, such as muscle and brain. Key components of mitochondrial biogenesis include factors like peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), which modulates multiple genes encoding mitochondrial proteins, and the translocase complexes essential for protein import into mitochondria, which help maintain mitochondrial function and homeostasis (MacPherson et al.). Furthermore, the dynamic nature of mitochondrial biogenesis underscores the complexity of mitochondrial roles beyond mere ATP production, as it plays a vital part in cellular health and adaptation to metabolic changes, ultimately influencing organismal physiology (Enriquez et al.).

Factor	Impact_on_Biogenesis	Mechanism	Source
Exercise	Increases	Enhances PGC-1α expression	Harvard Medical School
Caloric Restriction	Increases	Stimulates SIRT1 activation	Nature Reviews Molecular Cell Biology
Aging	Decreases	Reduced PGC-1α levels	Cell Metabolism
Nutrient Availability	Varies	Depends on the type of nutrients (e.g., amino acids, glucose)	Annual Review of Nutrition
Oxidative Stress	Decreases	Inhibits mitochondrial transcription factors	Free Radical Biology and Medicine

Mitochondrial Biogenesis Regulation Factors

C. The role of mitochondria in apoptosis and cell signaling

Mitochondria play a pivotal role in orchestrating both apoptosis and cellular signaling, acting as critical hubs for metabolic and regulatory functions within the cell. Apoptosis, or programmed cell death, is intricately linked to mitochondrial function, particularly through the release of pro-apoptotic factors like cytochrome c, which triggers the activation of caspases, a family of proteases essential for cell death (cite29). Additionally, mitochondria contribute to cellular signaling pathways by modulating reactive oxygen species (ROS) production. As highlighted in recent studies, activation of small GTPases such as Rac leads to ROS generation, which in turn influences signaling pathways like NF-kB activation, ultimately affecting gene expression and cellular responses (cite30). This dual role underscores the importance of mitochondrial dynamics in maintaining cellular homeostasis and dictating outcomes during stress conditions, effectively positioning mitochondria as critical players in both survival and apoptosis pathways within the intricate cellular landscape.

This chart presents an overview of the various roles that mitochondria play in cellular functions. It categorizes these roles into three main areas: Mitochondrial Role, Cell Signaling Role, and Mitochondrial Dynamics. Each category highlights the number of aspects, mechanisms, and influences key to understanding mitochondrial functions, demonstrating the critical contributions of mitochondria in cellular health and signaling.

IV. Conclusion

In conclusion, the study of mitochondria reveals their integral role not only as the cells primary energy producers but also as critical players in cellular adaptability and survival mechanisms under varying conditions. As demonstrated, the dynamic relationship between mitochondria and lipid droplets (LDs) underscores their collaborative efforts during nutrient scarcity, wherein increased interactions enhance fatty acid supply for mitochondrial beta-oxidation, revealing a highly regulated cellular network ((Bosch et al.)). Furthermore, the protective mechanisms that sustain mitochondrial function amid cellular stress, exemplified by the role of A1M in mitigating oxidative damage and preserving ATP production, illustrate the mitochondrias resilience during cell death processes ((Fellman et al.)). Collectively, these insights reinforce the significance of mitochondria beyond mere energy conversion; they are vital in orchestrating cellular responses that maintain homeostasis and support life, thus solidifying their status as the true powerhouses of the cell.

A. Summary of key points discussed

The discussion surrounding mitochondria provides critical insights into their multifaceted roles beyond mere energy production. First and foremost, mitochondria are pivotal in regulating cellular metabolism, acting as metabolic hubs where enzymatic activities correlate with cellular energy demands. Furthermore, their involvement in apoptosis highlights their essential function in maintaining cellular health and homeostasis. Recent research indicates that mitochondrial health is linked to psychological stressors, suggesting that emotional states can influence mitochondrial functionality. For instance, a study demonstrated that caregivers facing chronic stress exhibited lower mitochondrial health index (MHI) scores, underscoring a direct relationship between mood and mitochondrial capacity (Aschbacher et al.). Additionally, the aging process has been closely tied to mitochondrial performance, reinforcing the idea that these organelles are integral to age-related cellular changes (Haas et al.). Thus, the dynamic interplay between mitochondria, metabolism, and emotional health emerges as a compelling narrative in understanding cellular function.

B. Implications of mitochondrial research for medicine

Mitochondrial research has profound implications for medicine, particularly in the understanding and treatment of various diseases, including neurodegenerative disorders such as Alzheimer’s disease. Evidence suggests that impaired mitochondrial function and glucose hypometabolism play a critical role in the pathogenesis of Alzheimer’s, where increased activity of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) has been linked to reduced glucose oxidation in neurons (Arsenian et al.). This bioenergetic deficit not only affects neuronal health but also highlights potential therapeutic avenues through the use of nutraceutical compounds, which may recover mitochondrial function. Additionally, studies have shown that mitochondrial dysfunction mediated by mitogen-activated protein kinases, particularly JNK2, contributes to hepatic injury after hemorrhagic shock, suggesting that targeting these pathways could mitigate damage and improve recovery outcomes (Czerny et al.). Thus, advancements in mitochondrial research are paving the way for innovative strategies in disease management and therapy.

C. Future directions in mitochondrial studies

As research into mitochondrial biology continues to evolve, future directions in mitochondrial studies promise to unveil critical insights into cellular metabolism, disease mechanisms, and therapeutic interventions. One promising avenue is the exploration of mitochondrial dynamics, particularly how mitochondrial fission and fusion processes influence health and disease states. Understanding these dynamics could illuminate their roles in neurodegenerative disorders and metabolic diseases, potentially leading to innovative treatment strategies. Additionally, the advent of advanced imaging techniques and genomics will enable scientists to investigate mitochondrial function in real-time and at unprecedented resolution, fostering a more nuanced understanding of mitochondrial interaction with cellular organelles. Furthermore, expanding research into the influence of mitochondrial epigenetics may reveal how environmental factors affect mitochondrial function over generations, underscoring the mitochondrias role not only in energy production but also in broader biological contexts. Ultimately, these future explorations hold the potential to significantly impact both basic biology and clinical applications.

References

• Haas, Richard H. “Mitochondrial Dysfunction in Aging and Diseases of Aging.”. eScholarship, University of California, 2019, https://core.ac.uk/download/323065598.pdf
• Aschbacher, Kirstin, Burelle, Yan, Coccia, Michael, Cuillerier, et al.. “A Mitochondrial Health Index Sensitive to Mood and Caregiving Stress.”. eScholarship, University of California, 2018, https://core.ac.uk/download/323062942.pdf
• Pearce, E., Rambold, A.. “Mitochondrial Dynamics at the Interface of Immune Cell Metabolism and Function”. ‘Elsevier BV’, 2018,
• Deighton, R.F., Herrmann, A.G., Kerr, L.E., Le Bihan, et al.. “Adaptive changes in the neuronal proteome: mitochondrial energy production, endoplasmic reticulum stress, and ribosomal dysfunction in the cellular response to metabolic stress”. ‘Springer Science and Business Media LLC’, 2013, https://core.ac.uk/download/16459694.pdf
• Alex Dyson, Audibert G, Berne RM, Blitzer ML, Boutilier RG, Brown IP, Devlin C, et al.. “The key role of nitric oxide in hypoxia: hypoxic vasodilation and energy supply-demand matching”. ‘Mary Ann Liebert Inc’, 2013,
• Atchison, Birky, Carelli, Castellino, Chinnery, Francis L. Martin, Ioannides, et al.. “Underlying role of mitochondrial mutagenesis in the pathogenesis of a disease and current approaches for translational research”. ‘Oxford University Press (OUP)’, 2016, https://core.ac.uk/download/74206192.pdf
• Lucas, Millikin, Narendra, Santel, Zhang. “The Interplay among PINK1/PARKIN/Dj-1 Network during Mitochondrial Quality Control in Cancer Biology: Protein Interaction Analysis”. ‘MDPI AG’, 2018, https://core.ac.uk/download/287581184.pdf
• Chen, Thomas C, Gonzalez, Reyna, Hofman, Florence M, Louie, et al.. “Repositioning of Verrucosidin, a purported inhibitor of chaperone protein GRP78, as an inhibitor of mitochondrial electron transport chain complex I.”. eScholarship, University of California, 2013, https://core.ac.uk/download/323067756.pdf
• Abdul, Appleby, Armstrong, Bai, Bourges, Buchet, Chai, et al.. “Alterations of the mitochondrial proteome caused by the absence of mitochondrial DNA: A proteomic view”. ‘Wiley’, 2006, https://core.ac.uk/download/52704201.pdf
• Alvarez, Silvia, Astiz, Mariana, Imsen, Mercedes, Magnani, et al.. “Hormone deprivation alters mitochondrial function and lipid profile in the hippocampus”. BioScientifica, 2017, https://core.ac.uk/download/159286401.pdf
• Anderton, Ryan S, Knuckey, Neville W, MacDougall, Gabriella, Mastaglia, et al.. “Mitochondria and neuroprotection in stroke: Cationic arginine-rich peptides (CARPs) as a novel class of mitochondria-targeted neuroprotective therapeutics”. ResearchOnline@ND, 2018, https://core.ac.uk/download/213607758.pdf
• Mansilla, Natanael, Radin, Ivan, Rödel, Gerhard, Steinebrunner, et al.. “The arabidopsis COX11 homolog is essential for cytochrome c oxidase activity”. ‘Frontiers Media SA’, 2015, https://core.ac.uk/download/159286718.pdf
• Adams, William P.. “Thyroid Hormone as a Method of Reducing Damage to Donor Hearts after Circulatory Arrest”. VCU Scholars Compass, 2017, https://core.ac.uk/download/84402524.pdf
• Jeena, M.T., Jin, Seongeon, Kim, Sangpil, Ryu, et al.. “Recent progress in mitochondria-targeted drug and drug-free agents for cancer therapy”. ‘MDPI AG’, 2019, https://core.ac.uk/download/289095010.pdf
• Chowanadisai, Winyoo, Clarke, Stephen, Guo, Xin, Lin, et al.. “Hypothalamic mitochondria in energy homeostasis and obesity”. ‘Open Access Text Pvt, Ltd.’, 2016, https://core.ac.uk/download/77979505.pdf
• Sarmidi, Mohamad Roji. “Food is our medicine”. 2012, https://core.ac.uk/download/11801185.pdf
• Forte, Maurizio, Migliarino, Serena, Perelli, Marika, Pierelli, et al.. “Uncoupling protein 2: a key player and a potential therapeutic target in vascular diseases”. ‘Hindawi Limited’, 2017, https://core.ac.uk/download/153367400.pdf
• Czerny, Christoph, Lehnert, Mark, Lemasters, John J., Maldonado, et al.. “C-Jun N-terminal kinase 2 promotes liver injury via the mitochondrial permeability transition after hemorrhage and resuscitation”. 2012, https://core.ac.uk/download/14526537.pdf
• Arsenian, Bateman, Beal, Bielarczyk, Blass, Bogaert, Bosetti, et al.. “BACE1 activity impairs neuronal glucose oxidation:rescue by beta-hydroxybutyrate and lipoic acid”. ‘Frontiers Media SA’, 2015, https://core.ac.uk/download/30664647.pdf
• Dang, Qing Ya, Fan, Xin Rong, Han, Chu Ting, Li, et al.. “Assessment of mitochondrial dysfunction and implications in cardiovascular disorders”. Elsevier, 2022, https://core.ac.uk/download/598039758.pdf
• Dacks, Joel B., Dorrell, Richard G., Richardson, Elizabeth, Tsaousis, et al.. “Evolutionary cell biology: Functional insight from “Endless forms most beautiful””. ‘American Society for Cell Biology (ASCB)’, 2015, https://core.ac.uk/download/30711862.pdf
• Khan, Mohsin, Kim, Seong-Jun, Siddiqui, Aleem, Syed, et al.. “Mitochondrial dynamics and viral infections: A close nexus.”. eScholarship, University of California, 2015, https://core.ac.uk/download/323064408.pdf
• Werb, Zena, Werner, Erica. “Integrins engage mitochondrial function for signal transduction by a mechanism dependent on Rho GTPases.”. eScholarship, University of California, 2002, https://core.ac.uk/download/323074866.pdf
• Bosch, Marta (Bosch Rodríguez), Enrich Bastús, Carles, Fajardo, Alba, Fernández-Vidal, et al.. “AMPK activation promotes lipid droplet dispersion on detyrosinated microtubules to increase mitochondrial fatty acid oxidation”. ‘Springer Science and Business Media LLC’, 2017, https://core.ac.uk/download/141524840.pdf
• Fellman, Vineta, Gram, Magnus, Kotarsky, Heike, Leanderson, et al.. “The radical-binding lipocalin A1M binds to a Complex I subunit and protects mitochondrial structure and function.”. ‘Mary Ann Liebert Inc’, 2013, https://core.ac.uk/download/83785446.pdf
• Oun, Asmaa. “Immune function of LRRK2:focus on mitochondrial metabolism”. ‘University of Groningen Press’, 2022, https://core.ac.uk/download/543462632.pdf
• Dumet, A., Rey, B., Romestaing, C., Roussel, et al.. “Oxidative phosphorylation efficiency, proton conductance and reactive oxygen species production of liver mitochondria correlates with body mass in frogs”. ‘The Company of Biologists’, 2015, https://core.ac.uk/download/42364842.pdf
• Kasi Ganeshan, T., Kasi Ganeshan, T.. “Investigating the protective role of the natural hormone Melatonin, in reducing drug-induced cardiotoxicity in the therapy of chronic diseases”. 2019, https://core.ac.uk/download/287605215.pdf
• Jiang, Nian, Li, Jian Jian, Wang, Shuangyan, Xie, et al.. “Cyclin B1/CDK1-regulated mitochondrial bioenergetics in cell cycle progression and tumor resistance.”. eScholarship, University of California, 2019, https://core.ac.uk/download/286361500.pdf
• Enriquez, Jose Antonio, Monzel, Anna S, Picard, Martin. “Multifaceted mitochondria: moving mitochondrial science beyond function and dysfunction.”. 2023, https://core.ac.uk/download/597466524.pdf
• MacPherson, Lisa, Tokatlidis, Konstantinos. “Protein trafficking in the mitochondrial intermembrane space: mechanisms and links to human disease”. ‘Portland Press Ltd.’, 2017, https://core.ac.uk/download/82958614.pdf