Mitochondrial dysfunction and oxidative stress in metabolic disorders - A Step towards mitochondria based therapeutic strategies

By Jasvinder Singh Bhatti, G. K. Bhatti, P. Reddy. Biochimica et Biophysica Acta - Molecular Basis of Disease, 2016

1,410 citations recorded by the source corpus.

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, 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.

Subfields: Clinical Biochemistry, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/369987b109111b68deaec02ae7177872079cbf3e

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Citations in the corpus

• Metabolic Syndrome: Updates on Pathophysiology and Management in 2021 (2022, background): “Thus, mitochondrial dysfunction can lead to ROS overproduction causing cell injury, the hallmark “oxidative stress” that contributes to the development of many disease processes including MetS [101].”
• Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives (2022, background): “The dysfunction of the mitochondria in these cells results in least formation of mitochondrial adenosine triphosphate which leads to the loss of glucose-stimulated insulin secretion [97,98].”
• Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “282,283 286 In light of these fi ndings, targeting mitochondrial pathways may represent a promising therapeutic strategy to mitigate the pathological consequences of metabolic syndrome.”
• PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism (2020, background): “PGC-1α leads to the activation of several transcription factors including nuclear respiratory factors (NRF-1 and 2), PPARs, mitochondrial transcription factor A (Tfam), and ERRα to increase transcription of genes related to mitochondrial biogenesis and function [66, 67].”