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Ratiometric Biosensors that Measure Mitochondrial Redox State and ATP in Living Yeast Cells
Published on: July 22, 2013
Regulatory role of mitochondria in oxidative stress and atherosclerosis
Jui-Chih Chang1, Shou-Jen Kou, Wei-Ting Lin
1Jui-Chih Chang, Wei-Ting Lin, Chin-San Liu, Department of Neurology, Vascular and Genomic Center, Changhua Christian Hospital, Changhua 50094, Taiwan, China.
Abstract:
Mitochondrial physiology and biogenesis play a crucial role in the initiation and progression of cardiovascular disease following oxidative stress-induced damage such as atherosclerosis (AST). Dysfunctional mitochondria caused by an increase in mitochondrial reactive oxygen species (ROS) production, accumulation of mitochondrial DNA damage, and respiratory chain deficiency induces death of endothelial/smooth muscle cells and favors plaque formation/rupture via the regulation of mitochondrial biogenesis-related genes such as peroxisome proliferator-activated receptor γ coactivator (PGC-1), although more detailed mechanisms still need further study. Based on the effect of healthy mitochondria produced by mitochondrial biogenesis on decreasing ROS-mediated cell death and the recent finding that the regulation of PGC-1 involves mitochondrial fusion-related protein (mitofusin), we thus infer the regulatory role of mitochondrial fusion/fission balance in AST pathophysiology. In this review, the first section discusses the possible association between AST-inducing factors and the molecular regulatory mechanisms of mitochondrial biogenesis and dynamics, and explains the role of mitochondria-dependent regulation in cell apoptosis during AST development. Furthermore, nitric oxide has the Janus-faced effect by protecting vascular damage caused by AST while being a reactive nitrogen species (RNS) which act together with ROS to damage cells. Therefore, in the second section we discuss mitochondrial ATP-sensitive K(+) channels, which regulate mitochondrial ion transport to maintain mitochondrial physiology, involved in the regulation of ROS/RNS production and their influence on AST/cardiovascular diseases (CVD). Through this review, we can further appreciate the multi-regulatory functions of the mitochondria involved in AST development. The understanding of these related mechanisms will benefit drug development in treating AST/CVD through targeted biofunctions of mitochondria.
Insights
Mitochondrial health is vital in cardiovascular disease. This review explores how mitochondrial dynamics, biogenesis, and ion channels influence atherosclerosis (AST) and cardiovascular diseases (CVD), offering insights for targeted drug development.
Area of Science:
- Cardiovascular Research
- Mitochondrial Biology
- Pathophysiology
Background:
- Oxidative stress and mitochondrial dysfunction are key drivers of atherosclerosis (AST) and cardiovascular disease (CVD).
- Mitochondrial reactive oxygen species (ROS) production, DNA damage, and respiratory chain defects contribute to endothelial cell death and plaque instability.
- Mitochondrial biogenesis, regulated by factors like peroxisome proliferator-activated receptor γ coactivator (PGC-1), influences cell survival and AST progression.
Purpose of the Study:
- To review the molecular mechanisms linking AST-inducing factors to mitochondrial biogenesis and dynamics.
- To elucidate the role of mitochondrial fusion/fission balance in AST pathophysiology.
- To discuss the dual role of nitric oxide and the influence of mitochondrial ATP-sensitive K(+) channels on ROS/RNS production in AST/CVD.
Main Methods:
- Literature review focusing on mitochondrial regulation in cardiovascular disease.
- Analysis of molecular mechanisms of mitochondrial biogenesis and dynamics in atherosclerosis.
- Discussion of the interplay between ROS/RNS, nitric oxide, and mitochondrial ion channels in cardiovascular pathology.
Main Results:
- Mitochondrial dysfunction, including increased ROS and impaired biogenesis, exacerbates AST development.
- Mitochondrial fusion/fission balance is inferred to play a regulatory role in AST pathophysiology.
- Mitochondrial ATP-sensitive K(+) channels are involved in regulating ROS/RNS production impacting AST/CVD.
Conclusions:
- Mitochondria are central regulators of cell apoptosis and plaque development in AST.
- Understanding mitochondrial dynamics and biogenesis offers therapeutic targets for AST/CVD.
- Targeting mitochondrial biofunctions holds promise for novel drug development in cardiovascular medicine.
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