ReviewAdvances in experimental medicine and biology2017
Mitochondrial Proton Leak Plays a Critical Role in Pathogenesis of Cardiovascular Diseases.
Review in Advances in experimental medicine and biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 1 of them a synthesis that pooled it.
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Who cites it
111 citing papers in PubMed, 1 synthesis or guideline pooled it, 170 citations in OpenAlex.
- Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection.Basic research in cardiology · 2018Guideline
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- Detection of mitochondrial bioenergetics using a novel bimodal 3D microelectrode array (MEA)-based biosensor.Microsystems & nanoengineering · 2026Article
- Cardiac Mitochondrial Dysfunction Following Bleomycin-Induced Acute Lung Injury in Rats.bioRxiv : the preprint server for biology · 2026Article
- Novel Organelle-Based Intracellular Immunity with Mechanistic and Therapeutic Implications.Barrier immunity · 2026Article
- Effects of Cannabidiol on TAFAZZIN-Deficient B-Lymphoblastoid Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Reversible dissociation of mitochondrial Complex V balances anabolic and energy-generating needs in cancer.iScience · 2026Article
- Sex-dependent differences in bioenergetics of young mouse brain microvasculature: implications for oxygen-glucose deprivation and reoxygenation injury.American journal of physiology. Heart and circulatory physiology · 2026Article
- Mitochondrial Metabolic Reprogramming of Cortical Neurons by Prenatal Exposure to Corticosterone: A Shift from ATP Synthesis to Membrane Potential Maintenance.Experimental neurobiology · 2026Article
- New Insight Into Male Infertility: Deviation From Basic Tenets of Life.Oxidative medicine and cellular longevity · 2026Review
- Mitochondrial respiratory activity and DNA damage in peripheral blood mononuclear cells in borderline personality disorder.Psychological medicine · 2025Article
- Non-invasive bioelectrical therapy suppresses retinal neovascularization by modulating cellular metabolism and inflammation.Cell communication and signaling : CCS · 2025Article
- Exploring Immediate Photon Effects From 635 nm Light on Mitochondrial Bioenergetics.Journal of biophotonics · 2025Article
- A Pharmacological Dose of Liraglutide Improves Mitochondrial Performance in Mouse Leydig Cells.International journal of molecular sciences · 2025Article
- Bee Venom Proteins Enhance Proton Absorption by Membranes Composed of Phospholipids of the Myelin Sheath and Endoplasmic Reticulum: Pharmacological Relevance.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Combined Effects of Exercise and Vitamin D on Neuroinflammation, Blood-Brain Barrier Integrity, Oxidative Stress, and Cognitive Function in Nonpathological Mice.International neurourology journal · 2025Article
- Epicatechin DecreasesInternational journal of molecular sciences · 2025Article
- Myeloma mesenchymal stem cells' bioenergetics afford a novel selective therapeutic target.Oncogenesis · 2025Article
- Supplementation with aspalathin and sulforaphane protects cultured cardiac cells against dyslipidemia-associated oxidative damage.Metabolism open · 2025Article
- Mitochondrial Localization and Function of Adenosine Receptors.International journal of biological sciences · 2025Article
51 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondrial proton leak is the principal mechanism that incompletely couples substrate oxygen to ATP generation. This chapter briefly addresses the recent progress made in understanding the role of proton leak in the pathogenesis of cardiovascular diseases. Majority of the proton conductance is mediated by uncoupling proteins (UCPs) located in the mitochondrial inner membrane. It is evident that the proton leak and reactive oxygen species (ROS) generated from electron transport chain (ETC) in mitochondria are linked to each other. Increased ROS production has been shown to induce proton conductance, and in return, increased proton conductance suppresses ROS production, suggesting the existence of a positive feedback loop that protects the biological systems from detrimental effects of augmented oxidative stress. There is mounting evidence attributing to proton leak and uncoupling proteins a crucial role in the pathogenesis of cardiovascular disease. We can surmise the role of "uncoupling" in cardiovascular disorders as follows; First, the magnitude of the proton leak and the mechanism involved in mediating the proton leak determine whether there is a protective effect against ischemia-reperfusion (IR) injury. Second, uncoupling by UCP2 preserves vascular function in diet-induced obese mice as well as in diabetes. Third, etiology determines whether the proton conductance is altered or not during hypertension. And fourth, proton leak regulates ATP synthesis-uncoupled mitochondrial ROS generation, which determines pathological activation of endothelial cells for recruitment of inflammatory cells. Continue effort in improving our understanding in the role of proton leak in the pathogenesis of cardiovascular and metabolic diseases would lead to identification of novel therapeutic targets for treatment.
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