Mitochondrial dysfunction and oxidative stress in metabolic disorders - A step towards mitochondria based therapeutic strategies.
Mitochondria are the powerhouses of the cell and are involved in essential functions of the cell, including ATP production, intracellular Ca2+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.
Department of Biotechnology and Bioinformatics, Sri Guru Gobind Singh College, Sector-26, Chandigarh 160019, India; Garrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States. Electronic address: jasvinderbhatti@yahoo.com.
Jasvinder Singh
JS
Bhatti
UGC Centre of Excellence in Nano applications, Panjab University, UIPS building, Chandigarh 160014, India.
Gurjit Kaur
GK
Bhatti
Garrison Institute on Aging, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Cell Biology & Biochemistry Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Neuroscience & Pharmacology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Neurology Department, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Speech, Language and Hearing Sciences Departments, Texas Tech University Health Sciences Center, 3601 4th Street, MS 9424, Lubbock, TX 79430, United States; Garrison Institute on Aging, South West Campus, Texas Tech University Health Sciences Center, 6630 S. Quaker Suite E, MS 7495, Lubbock, TX 79413, United States.
P Hemachandra
PH
Reddy
D000818:Animals; D006801:Humans; D008659:Metabolic Diseases / Q000378:metabolism* / Q000473:pathology / Q000628:therapy*; D008928:Mitochondria / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress
Cardiovascular disease; Metabolic syndrome; Mitochondria; Mitochondria-targeted antioxidants; Obesity; Oxidative stress; Pre-diabetes; Reactive oxygen species; Type-2-diabetes