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Mitochondrial Metabolism and Function in Health and Disease
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Mitochondrial Metabolism and Function in Health and Disease

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: 15 September 2024 | Viewed by 26579

Special Issue Editors

Prof. Dr. Pilar Roca

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Guest Editor
1. Grupo Multidisciplinar de Oncología Traslacional, Institut Universitari d’Investigació en Ciències de la Salut (IUNICS), Universitat de les Illes Balears, E-07122 Palma, Spain
2. Instituto de Investigación Sanitaria Illes Balears (IdISBa), Hospital Universitario Son Espases, Edificio S, E-07120 Palma, Spain
3. Ciber Fisiopatología Obesidad y Nutrición (CB06/03), Instituto Salud Carlos III, E-28029 Madrid, Spain
Interests: mitochondrial function; metabolism; colorectal cancer; breast cancer; oxidative stress
Prof. Dr. Jordi Oliver

E-Mail Website
Guest Editor
Department of Fundamental Biology and Health Sciences, University of the Balearic Islands, Cra de Valldemossa, 07122 Palma de Mallorca, Spain
Interests: mitochondrial function; metabolism; colorectal cancer; breast cancer; oxidative stress
Dr. Margalida Torrens-Mas

E-Mail Website
Guest Editor
Vascular and Metabolic Pathologies, Health Research Institute of the Balearic Islands (IdISBa), Palma, Spain
Interests: mitochondrial function; metabolism; cancer; oxidative stress; biological aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Mitochondria are involved in multiple functions in the cell, including energy metabolism, calcium homeostasis, regulation of redox status, and cell death, among others. Thus, the maintenance of mitochondrial homeostasis is critical for cell survival and is tightly regulated by several processes, including mitochondrial biogenesis, mitochondrial dynamics, and mitophagy. This way, the mitochondrial network is continuously restructured while damaged mitochondria are removed, keeping a healthy pool of mitochondria. Mitochondrial dysfunction can occur when one or more of these processes is altered and can ultimately compromise cell metabolism and function. It has been described that mitochondrial dysfunction contributes to several diseases, such as cancer, obesity, or diabetes, and has also been involved in the hallmarks of aging.

This Special Issue, titled “Mitochondrial Metabolism and Function in Health and Disease”, aims to highlight the latest advances in this research topic. We invite authors to submit original research papers and review articles analyzing the contribution of mitochondrial metabolism and function to the development of different pathologies and potential therapeutic strategies to counteract mitochondrial dysfunction.

Prof. Dr. Pilar Roca
Prof. Dr. Jordi Oliver
Dr. Margalida Torrens-Mas
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • mitochondrial function
  • mitochondrial metabolism
  • mitochondrial biogenesis
  • mitophagy
  • mitochondrial dynamics
  • mitochondrial disease
  • cancer
  • aging
  • obesity

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Published Papers (10 papers)

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Research

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21 pages, 2327 KiB  
Article
Effect of CB1 Receptor Deficiency on Mitochondrial Quality Control Pathways in Gastrocnemius Muscle
by Rosalba Senese, Giuseppe Petito, Elena Silvestri, Maria Ventriglia, Nicola Mosca, Nicoletta Potenza, Aniello Russo, Francesco Manfrevola, Gilda Cobellis, Teresa Chioccarelli, Veronica Porreca, Vincenza Grazia Mele, Rosanna Chianese, Pieter de Lange, Giulia Ricci, Federica Cioffi and Antonia Lanni
Biology 2024, 13(2), 116; https://doi.org/10.3390/biology13020116 - 11 Feb 2024
Viewed by 1953
Abstract
This study aims to explore the complex role of cannabinoid type 1 receptor (CB1) signaling in the gastrocnemius muscle, assessing physiological processes in both CB1+/+ and CB1−/− mice. The primary focus is to enhance our understanding of how CB1 contributes to [...] Read more.
This study aims to explore the complex role of cannabinoid type 1 receptor (CB1) signaling in the gastrocnemius muscle, assessing physiological processes in both CB1+/+ and CB1−/− mice. The primary focus is to enhance our understanding of how CB1 contributes to mitochondrial homeostasis. At the tissue level, CB1−/− mice exhibit a substantial miRNA-related alteration in muscle fiber composition, characterized by an enrichment of oxidative fibers. CB1 absence induces a significant increase in the oxidative capacity of muscle, supported by elevated in-gel activity of Complex I and Complex IV of the mitochondrial respiratory chain. The increased oxidative capacity is associated with elevated oxidative stress and impaired antioxidant defense systems. Analysis of mitochondrial biogenesis markers indicates an enhanced capacity for new mitochondria production in CB1−/− mice, possibly adapting to altered muscle fiber composition. Changes in mitochondrial dynamics, mitophagy response, and unfolded protein response (UPR) pathways reveal a dynamic interplay in response to CB1 absence. The interconnected mitochondrial network, influenced by increased fusion and mitochondrial UPR components, underlines the dual role of CB1 in regulating both protein quality control and the generation of new mitochondria. These findings deepen our comprehension of the CB1 impact on muscle physiology, oxidative stress, and MQC processes, highlighting cellular adaptability to CB1−/−. This study paves the way for further exploration of intricate signaling cascades and cross-talk between cellular compartments in the context of CB1 and mitochondrial homeostasis. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Function in Health and Disease)
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13 pages, 2537 KiB  
Article
Mitochondrial Functionality Is Regulated by Alkylphospholipids in Human Colon Cancer Cells
by Margalida Torrens-Mas, Alejandro Collado-Solé, Alberto Sola-Leyva, María Paz Carrasco-Jiménez, Jordi Oliver, Daniel Gabriel Pons, Pilar Roca and Jorge Sastre-Serra
Biology 2023, 12(12), 1457; https://doi.org/10.3390/biology12121457 - 22 Nov 2023
Cited by 1 | Viewed by 1580
Abstract
Alkylphospholipids (APLs) have been studied as anticancer drugs that interfere with biological membranes without targeting DNA. Although their mechanism of action is not fully elucidated yet, it is known that they disrupt the intracellular trafficking of cholesterol and its metabolism. Here, we analyzed [...] Read more.
Alkylphospholipids (APLs) have been studied as anticancer drugs that interfere with biological membranes without targeting DNA. Although their mechanism of action is not fully elucidated yet, it is known that they disrupt the intracellular trafficking of cholesterol and its metabolism. Here, we analyzed whether APLs could also interfere with mitochondrial function. For this purpose, we used HT29 colorectal cancer cells, derived from a primary tumor, and SW620 colorectal cancer cells, derived from a metastasis site. After treatment with the APLs miltefosine and perifosine, we analyzed various mitochondrial parameters, including mitochondrial mass, cardiolipin content, mitochondrial membrane potential, H2O2 production, the levels of oxidative phosphorylation (OXPHOS) complexes, metabolic enzymes activity, the oxygen consumption rate, and the levels of apoptosis and autophagy markers. APLs, especially perifosine, increased mitochondrial mass while OXPHOS complexes levels were decreased without affecting the total oxygen consumption rate. Additionally, we observed an increase in pyruvate dehydrogenase (PDH) and isocitrate dehydrogenase (IDH) levels and a decrease in lactate dehydrogenase (LDH) activity, suggesting a metabolic rewiring induced by perifosine. These alterations led to higher mitochondrial membrane potential, which was potentiated by decreased uncoupling protein 2 (UCP2) levels and increased reactive oxygen species (ROS) production. Consequently, perifosine induced an imbalance in mitochondrial function, resulting in higher ROS production that ultimately impacted cellular viability. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Function in Health and Disease)
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16 pages, 2811 KiB  
Article
Remodelling of the Mitochondrial Bioenergetic Pathways in Human Cultured Fibroblasts with Carbohydrates
by Margherita Protasoni and Jan-Willem Taanman
Biology 2023, 12(7), 1002; https://doi.org/10.3390/biology12071002 - 14 Jul 2023
Cited by 1 | Viewed by 1543
Abstract
Mitochondrial oxidative phosphorylation defects underlie many neurological and neuromuscular diseases. Patients’ primary dermal fibroblasts are one of the most commonly used in vitro models to study mitochondrial pathologies. However, fibroblasts tend to rely more on glycolysis than oxidative phosphorylation for their energy when [...] Read more.
Mitochondrial oxidative phosphorylation defects underlie many neurological and neuromuscular diseases. Patients’ primary dermal fibroblasts are one of the most commonly used in vitro models to study mitochondrial pathologies. However, fibroblasts tend to rely more on glycolysis than oxidative phosphorylation for their energy when cultivated in standard high-glucose medium, rendering it difficult to expose mitochondrial dysfunctions. This study aimed to systematically investigate to which extent the use of galactose- or fructose-based medium switches the fibroblasts’ energy metabolism to a more oxidative state. Highly proliferative cells depend more on glycolysis than less proliferative cells. Therefore, we investigated two primary dermal fibroblast cultures from healthy subjects: a highly proliferative neonatal culture and a slower-growing adult culture. Cells were cultured with 25 mM glucose, galactose or fructose, and 4 mM glutamine as carbon sources. Compared to glucose, both galactose and fructose reduce the cellular proliferation rate, but the galactose-induced drop in proliferation is much more profound than the one observed in cells cultivated in fructose. Both galactose and fructose result in a modest increase in mitochondrial content, including mitochondrial DNA, and a disproportionate increase in protein levels, assembly, and activity of the oxidative phosphorylation enzyme complexes. Galactose- and fructose-based media induce a switch of the prevalent biochemical pathway in cultured fibroblasts, enhancing aerobic metabolism when compared to glucose-based medium. While both galactose and fructose stimulate oxidative phosphorylation to a comparable degree, galactose decreases the cellular proliferation rate more than fructose, suggesting that a fructose-based medium is a better choice when studying partial oxidative phosphorylation defects in patients’ fibroblasts. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Function in Health and Disease)
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23 pages, 3820 KiB  
Article
Mitochondrial Proteome Changes in Rett Syndrome
by Gocha Golubiani, Laura van Agen, Lia Tsverava, Revaz Solomonia and Michael Müller
Biology 2023, 12(7), 956; https://doi.org/10.3390/biology12070956 - 3 Jul 2023
Cited by 1 | Viewed by 2132
Abstract
Rett syndrome (RTT) is a genetic neurodevelopmental disorder with mutations in the X-chromosomal MECP2 (methyl-CpG-binding protein 2) gene. Most patients are young girls. For 7–18 months after birth, they hardly present any symptoms; later they develop mental problems, a lack of communication, irregular [...] Read more.
Rett syndrome (RTT) is a genetic neurodevelopmental disorder with mutations in the X-chromosomal MECP2 (methyl-CpG-binding protein 2) gene. Most patients are young girls. For 7–18 months after birth, they hardly present any symptoms; later they develop mental problems, a lack of communication, irregular sleep and breathing, motor dysfunction, hand stereotypies, and seizures. The complex pathology involves mitochondrial structure and function. Mecp2−/y hippocampal astrocytes show increased mitochondrial contents. Neurons and glia suffer from oxidative stress, a lack of ATP, and increased hypoxia vulnerability. This spectrum of changes demands comprehensive molecular studies of mitochondria to further define their pathogenic role in RTT. Therefore, we applied a comparative proteomic approach for the first time to study the entity of mitochondrial proteins in a mouse model of RTT. In the neocortex and hippocampus of symptomatic male mice, two-dimensional gel electrophoresis and subsequent mass-spectrometry identified various differentially expressed mitochondrial proteins, including components of respiratory chain complexes I and III and the ATP-synthase FoF1 complex. The NADH-ubiquinone oxidoreductase 75 kDa subunit, NADH dehydrogenase [ubiquinone] iron-sulfur protein 8, NADH dehydrogenase [ubiquinone] flavoprotein 2, cytochrome b-c1 complex subunit 1, and ATP synthase subunit d are upregulated either in the hippocampus alone or both the hippocampus and neocortex of Mecp2−/y mice. Furthermore, the regulatory mitochondrial proteins mitofusin-1, HSP60, and 14-3-3 protein theta are decreased in the Mecp2−/y neocortex. The expressional changes identified provide further details of the altered mitochondrial function and morphology in RTT. They emphasize brain-region-specific alterations of the mitochondrial proteome and support the notion of a metabolic component of this devastating disorder. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Function in Health and Disease)
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13 pages, 1780 KiB  
Article
S-15176 Difumarate Salt Can Impair Mitochondrial Function through Inhibition of the Respiratory Complex III and Permeabilization of the Inner Mitochondrial Membrane
by Natalia V. Belosludtseva, Vlada S. Starinets, Alena A. Semenova, Anastasia D. Igoshkina, Mikhail V. Dubinin and Konstantin N. Belosludtsev
Biology 2022, 11(3), 380; https://doi.org/10.3390/biology11030380 - 27 Feb 2022
Cited by 2 | Viewed by 2336
Abstract
S-15176 difumarate salt, a derivative of the anti-ischemic metabolic drug trimetazidine, has been intensively studied for its impact on cellular metabolism in animal models of ischemia-reperfusion injury of the liver, heart, spinal cord, and other organs. Despite evidence of some reduction in oxidative [...] Read more.
S-15176 difumarate salt, a derivative of the anti-ischemic metabolic drug trimetazidine, has been intensively studied for its impact on cellular metabolism in animal models of ischemia-reperfusion injury of the liver, heart, spinal cord, and other organs. Despite evidence of some reduction in oxidative damage to cells, the results of therapy with S-15176 have been mostly disappointing, possibly because of the lack of data on its underlying mechanisms. Here, we aimed to investigate in more detail the role of complexes I-IV of the electron transport chain and membrane permeability transition in mitochondrial toxicity associated with S-15176. Using rat thymocyte and liver mitochondria, we demonstrated that: (1) acute exposure to S-15176 (10 to 50 μM) dose-dependently decreased the mitochondrial membrane potential; (2) S-15176 suppressed the ADP-stimulated (State 3) and uncoupled (State 3UDNP) respiration of mitochondria energized with succinate or malate/glutamate, but not ascorbate/TMPD, and increased the resting respiration (State 4) when using all the substrate combinations; (3) S-15176 directly inhibited the activity of the respiratory complex III; (4) low doses of S-15176 diminished the rate of H2O2 production by mitochondria; (5) at concentrations of above 30 μM, S-15176 reduced calcium retention capacity and contributed to mitochondrial membrane permeabilization. Taken together, these findings suggest that S-15176 at tissue concentrations reached in animals can impair mitochondrial function through suppression of the cytochrome bc1 complex and an increase in the nonspecific membrane permeability. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Function in Health and Disease)
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Review

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31 pages, 2124 KiB  
Review
Metformin: From Diabetes to Cancer—Unveiling Molecular Mechanisms and Therapeutic Strategies
by Emilia Amengual-Cladera, Pere Miquel Morla-Barcelo, Andrea Morán-Costoya, Jorge Sastre-Serra, Daniel Gabriel Pons, Adamo Valle, Pilar Roca and Mercedes Nadal-Serrano
Biology 2024, 13(5), 302; https://doi.org/10.3390/biology13050302 - 27 Apr 2024
Cited by 4 | Viewed by 2275
Abstract
Metformin, a widely used anti-diabetic drug, has garnered attention for its potential in cancer management, particularly in breast and colorectal cancer. It is established that metformin reduces mitochondrial respiration, but its specific molecular targets within mitochondria vary. Proposed mechanisms include inhibiting mitochondrial respiratory [...] Read more.
Metformin, a widely used anti-diabetic drug, has garnered attention for its potential in cancer management, particularly in breast and colorectal cancer. It is established that metformin reduces mitochondrial respiration, but its specific molecular targets within mitochondria vary. Proposed mechanisms include inhibiting mitochondrial respiratory chain Complex I and/or Complex IV, and mitochondrial glycerophosphate dehydrogenase, among others. These actions lead to cellular energy deficits, redox state changes, and several molecular changes that reduce hyperglycemia in type 2 diabetic patients. Clinical evidence supports metformin’s role in cancer prevention in type 2 diabetes mellitus patients. Moreover, in these patients with breast and colorectal cancer, metformin consumption leads to an improvement in survival outcomes and prognosis. The synergistic effects of metformin with chemotherapy and immunotherapy highlights its potential as an adjunctive therapy for breast and colorectal cancer. However, nuanced findings underscore the need for further research and stratification by molecular subtype, particularly for breast cancer. This comprehensive review integrates metformin-related findings from epidemiological, clinical, and preclinical studies in breast and colorectal cancer. Here, we discuss current research addressed to define metformin’s bioavailability and efficacy, exploring novel metformin-based compounds and drug delivery systems, including derivatives targeting mitochondria, combination therapies, and novel nanoformulations, showing enhanced anticancer effects. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Function in Health and Disease)
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12 pages, 592 KiB  
Review
The Role of Mitochondrial Dysfunction in Idiopathic Pulmonary Fibrosis: New Perspectives for a Challenging Disease
by Juan David Cala-Garcia, German Jose Medina-Rincon, Paula Andrea Sierra-Salas, Julio Rojano and Freddy Romero
Biology 2023, 12(9), 1237; https://doi.org/10.3390/biology12091237 - 14 Sep 2023
Cited by 2 | Viewed by 2226
Abstract
Mitochondrial biology has always been a relevant field in chronic diseases such as fibrosis or cancer in different organs of the human body, not to mention the strong association between mitochondrial dysfunction and aging. With the development of new technologies and the emergence [...] Read more.
Mitochondrial biology has always been a relevant field in chronic diseases such as fibrosis or cancer in different organs of the human body, not to mention the strong association between mitochondrial dysfunction and aging. With the development of new technologies and the emergence of new methodologies in the last few years, the role of mitochondria in pulmonary chronic diseases such as idiopathic pulmonary fibrosis (IPF) has taken an important position in the field. With this review, we will highlight the latest advances in mitochondrial research on pulmonary fibrosis, focusing on the role of the mitochondria in the aging lung, new proposals for mechanisms that support mitochondrial dysfunction as an important cause for IPF, mitochondrial dysfunction in different cell populations of the lung, and new proposals for treatment of the disease. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Function in Health and Disease)
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24 pages, 2394 KiB  
Review
35 Years of TFAM Research: Old Protein, New Puzzles
by Natalya Kozhukhar and Mikhail F. Alexeyev
Biology 2023, 12(6), 823; https://doi.org/10.3390/biology12060823 - 6 Jun 2023
Cited by 3 | Viewed by 3004
Abstract
Transcription Factor A Mitochondrial (TFAM), through its contributions to mtDNA maintenance and expression, is essential for cellular bioenergetics and, therefore, for the very survival of cells. Thirty-five years of research on TFAM structure and function generated a considerable body of experimental evidence, some [...] Read more.
Transcription Factor A Mitochondrial (TFAM), through its contributions to mtDNA maintenance and expression, is essential for cellular bioenergetics and, therefore, for the very survival of cells. Thirty-five years of research on TFAM structure and function generated a considerable body of experimental evidence, some of which remains to be fully reconciled. Recent advancements allowed an unprecedented glimpse into the structure of TFAM complexed with promoter DNA and TFAM within the open promoter complexes. These novel insights, however, raise new questions about the function of this remarkable protein. In our review, we compile the available literature on TFAM structure and function and provide some critical analysis of the available data. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Function in Health and Disease)
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15 pages, 1826 KiB  
Review
Glucose-Lowering Effects of Imeglimin and Its Possible Beneficial Effects on Diabetic Complications
by Hidekatsu Yanai, Hiroki Adachi, Mariko Hakoshima and Hisayuki Katsuyama
Biology 2023, 12(5), 726; https://doi.org/10.3390/biology12050726 - 16 May 2023
Cited by 6 | Viewed by 5039
Abstract
Mitochondrial dysfunction is a prominent pathological feature of type 2 diabetes, which contributes to β-cell mass reduction and insulin resistance. Imeglimin is a novel oral hypoglycemic agent with a unique mechanism of action targeting mitochondrial bioenergetics. Imeglimin reduces reactive oxygen species production, improves [...] Read more.
Mitochondrial dysfunction is a prominent pathological feature of type 2 diabetes, which contributes to β-cell mass reduction and insulin resistance. Imeglimin is a novel oral hypoglycemic agent with a unique mechanism of action targeting mitochondrial bioenergetics. Imeglimin reduces reactive oxygen species production, improves mitochondrial function and integrity, and also improves the structure and function of endoplasmic reticulum (ER), changes which enhance glucose-stimulated insulin secretion and inhibit the apoptosis of β-cells, leading to β-cell mass preservation. Further, imeglimin inhibits hepatic glucose production and ameliorates insulin sensitivity. Clinical trials into the effects of imeglimin monotherapy and combination therapy exhibited an excellent hypoglycemic efficacy and safety profile in type 2 diabetic patients. Mitochondrial impairment is closely associated with endothelial dysfunction, which is a very early event in atherosclerosis. Imeglimin improved endothelial dysfunction in patients with type 2 diabetes via both glycemic control-dependent and -independent mechanisms. In experimental animals, imeglimin improved cardiac and kidney function via an improvement in mitochondrial and ER function or/and an improvement in endothelial function. Furthermore, imeglimin reduced ischemia-induced brain damage. In addition to glucose-lowering effects, imeglimin can be a useful therapeutic option for diabetic complications in type 2 diabetic patients. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Function in Health and Disease)
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17 pages, 817 KiB  
Review
Sirtuin-3-Mediated Cellular Metabolism Links Cardiovascular Remodeling with Hypertension
by Jing Gao and Weili Shen
Biology 2023, 12(5), 686; https://doi.org/10.3390/biology12050686 - 6 May 2023
Cited by 1 | Viewed by 2249
Abstract
Hypertension can cause structural and functional abnormalities in the cardiovascular system, which can be attributed to both hemodynamic and nonhemodynamic factors. These alterations are linked with metabolic changes and are induced by pathological stressors. Sirtuins are enzymes that act as stress sensors and [...] Read more.
Hypertension can cause structural and functional abnormalities in the cardiovascular system, which can be attributed to both hemodynamic and nonhemodynamic factors. These alterations are linked with metabolic changes and are induced by pathological stressors. Sirtuins are enzymes that act as stress sensors and regulate metabolic adaptation by deacetylating proteins. Among them, mitochondrial SIRT3 performs a crucial role in maintaining metabolic homeostasis. Evidence from experimental and clinical studies has shown that hypertension-induced decreases in SIRT3 activity can lead to cellular metabolism reprogramming and, subsequently, increased susceptibility to endothelial dysfunction, myocardial hypertrophy, myocardial fibrosis, and heart failure. This review presents recent research advances in SIRT3-mediated metabolic adaptation in hypertensive cardiovascular remodeling. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Function in Health and Disease)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Autophagy regulates mitochondrial activities in cancer
Authors: Vaibhav Jain
Affiliation: Abramson Cancer Center and Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
Abstract: Autophagy is a multistep cellular recycling process that plays a multifaceted role in cancer. By degrading various macromolecules and organelles autophagy produces a variety of nutrients that help tumor growth and metastasis in the advanced stage of cancer. Mitochondria, the powerhouse of a cell produces most of the cellular energy which is consumed for multiple biological functions. In addition to the classical Warburg effect in cancer which generates energy via aerobic glycolysis, the role of mitochondrial derived energy via oxidative phosphorylation is also being appreciated for tumor growth. Recent advancements in autophagy and mitochondrial biology research indicate that the two processes are connected, and this interconnection plays an important role in cancer and other health disorders. This review will discuss how autophagy plays an important role in cancer by maintaining mitochondrial homeostasis and its functional capacities.

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