Mitochondrial dysfunction and oxidative stress in metabolic disorders - A step towards mitochondria based therapeutic strategies
Open accessAbstract
Mitochondria are the powerhouses of the cell and are involved in essential functions of the cell, including ATP production, intracellular Ca 2+ regulation, reactive oxygen species production & scavenging, regulation of apoptotic cell death and activation of the caspase family of proteases. Mitochondrial dysfunction and oxidative stress are largely involved in aging, cancer, age-related neurodegenerative and metabolic syndrome. In the last decade, tremendous progress has been made in understanding mitochondrial structure, function and their physiology in metabolic syndromes such as diabetes, obesity, stroke and hypertension, and heart disease. Further, progress has also been made in developing therapeutic strategies, including lifestyle interventions (healthy diet and regular exercise), pharmacological strategies and mitochondria-targeted approaches. These strategies were mainly focused to reduce mitochondrial dysfunction and oxidative stress and to maintain mitochondrial quality in metabolic syndromes. The purpose of our article is to highlight the recent progress on the mitochondrial role in metabolic syndromes and also summarize the progress of mitochondria-targeted molecules as therapeutic targets to treat metabolic syndromes. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.
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Mitochondrial dysfunction is both a cause and a consequence of metabolic disorders.
“mitochondrial dysfunction is both a cause and a consequence of metabolic disorders (Bhatti et al., 2017).”
From Comprehensive Multi-omics Analysis Reveals Mitochondrial Stress as a Central Biological Hub for Spaceflight Impact (2020) · cites this paper as Bhatti et al., 2017
A significant amount of ROS formed during mitochondrial dysfunction significantly contributes to the incidence of cardiovascular diseases.
“A significant amount of ROS formed during mitochondrial dysfunction significantly contributes to the incidence of cardiovascular diseases (Bhatti et al. 2017).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Bhatti et al. 2017
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- Authors
- Bhatti, J. S., Bhatti, G. K., & Reddy, P. H.
- Affiliations
- Sri Guru Gobind Singh College (IN)
- Panjab University (IN)
- Texas Tech University (US)
- Corresponding author
- Bhatti, Jasvinder Singh
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2017-05
- Volume
- 1863
- Issue
- 5
- Pages
- 1066-1077
- ISSN
- 0925-4439 (ISSN-L)
- PMC
- PMC5423868
- OpenAlex
- W2553902009
- Cited by
- 1,655
- References
- 238
- Citations by year
- 2026: 168 · 2025: 319 · 2024: 293 · 2023: 235 · 2022: 246 · 2021: 151 · 2020: 115 · 2019: 65 · 2018: 34 · 2017: 29
- FWCI
- 3.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (AG042178, AG047812)
- Garrison Family Foundation
- University Grants Commission, India (5-82/2016)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- mitochondrial dysfunction, oxidative stress, metabolic syndrome, mitochondrial-targeted therapy, reactive oxygen species, apoptosis, caspases, diabetes mellitus, obesity, hypertension, stroke, heart disease, mitochondrial quality, lifestyle intervention, pharmacotherapy
- MeSH terms
- Animals, Humans, Metabolic Diseases, Mitochondria, Oxidative Stress
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