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Published on: June 3, 2018
Multiple signaling pathways coordinately mediate reactive oxygen species dependent cardiomyocyte hypertrophy
Indira K Adiga1, Renuka R Nair
1Division of Cellular and Molecular Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, India.
Reactive oxygen species (ROS) induce cardiomyocyte hypertrophy by activating multiple pathways. Inhibiting any single pathway blocked ROS-induced cardiac cell growth, suggesting coordinated signaling in oxidative stress response.
Area of Science:
- Cardiovascular Biology
- Cellular Signaling
- Oxidative Stress Research
Background:
- Cardiac myocytes undergo hypertrophy in response to increased demand.
- Reactive oxygen species (ROS) are key mediators linking mechanical stimuli to cellular responses.
- Mitogen-activated protein kinase (MAPK), protein kinase C (PKC), and calcineurin are implicated in cardiac hypertrophy.
Purpose of the Study:
- To confirm the role of ROS in inducing cardiomyocyte hypertrophy.
- To investigate the contribution of specific signaling pathways in ROS-mediated cardiac hypertrophy.
Main Methods:
- Cultured newborn rat heart cells were used to study cellular responses.
- Enzyme-generated ROS (hypoxanthine-xanthine oxidase) were applied.
- Pathway-specific inhibitors were employed to dissect signaling mechanisms.
Main Results:
- ROS exposure led to cardiomyocyte hypertrophy.
- Inhibition of MAPK, PKC, or calcineurin individually prevented ROS-induced hypertrophy.
- This indicates a coordinated activation of these pathways by oxidative stress.
Conclusions:
- Oxidative stress is a significant inducer of cardiomyocyte hypertrophy.
- The hypertrophic response to ROS involves the coordinated action of MAPK, PKC, and calcineurin pathways.
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