Related Experiment Video
Updated: Aug 19, 2025
Author Spotlight: Uncovering the Role of Mitochondrial Calcium Phosphate in Heart Failure and Bioenergetics
Published on: August 23, 2024
Prohibitin1 maintains mitochondrial quality in isoproterenol-induced cardiac hypertrophy in H9C2 cells
Moumita Chakrabarti1,2, Ganesh Kumar Raut1,2, Nishant Jain1,2
1Applied Biology Department, CSIR-Indian Institute of Chemical Technology, Hyderabad, Telangana, India.
Insights
Prohibitin1 (PHB1) protects against cardiac hypertrophy by maintaining mitochondrial quality. Inducing PHB1 may offer new therapies for heart conditions.
Area of Science:
- Mitochondrial biology
- Cardiovascular research
- Cellular stress response
Background:
- Cardiac hypertrophy (CH) progresses from adaptive to maladaptive states under persistent stress.
- Prohibitin1 (PHB1) shows protective effects against CH-induced oxidative stress.
- The precise mechanism of PHB1's protective role in CH, particularly its mitochondrial function, requires elucidation.
Purpose of the Study:
- To investigate the hypothesis that PHB1 maintains mitochondrial quality in cardiac hypertrophy (CH).
- To elucidate the role of PHB1 in mitochondrial quality control pathways during CH.
Main Methods:
- Cardiac hypertrophy (CH) was induced using Isoproterenol (ISO) in H9C2 cells overexpressing PHB1.
- Mitochondrial quality control pathways were analyzed in treated cells.
Main Results:
- PHB1 overexpression attenuated ISO-induced CH and restored mitochondrial morphology.
- PHB1 blocked the IGF1R/AKT pathway and preserved mitochondrial membrane potential.
- PHB1 enhanced mitochondrial biogenesis, improved respiratory capacity, and promoted mitophagy.
Conclusions:
- PHB1 plays a crucial role in maintaining mitochondrial quality in ISO-induced CH.
- PHB1's protective effects involve regulating mitochondrial morphology, membrane potential, biogenesis, respiration, and mitophagy.
- Inducing PHB1 in cardiac cells presents a potential therapeutic strategy for CH.
Background Information:
Various types of stress initially induce a state of cardiac hypertrophy (CH) in the heart. But, persistent escalation of cardiac stress leads to progression from an adaptive physiological to a maladaptive pathological state. So, elucidating molecular mechanisms that can attenuate CH is imperative in developing cardiac therapies. Previously, we showed that Prohibitin1 (PHB1) has a protective role in CH-induced oxidative stress. Nevertheless, it is unclear how PHB1, a mitochondrial protein, has a protective role in CH. Therefore, we hypothesized that PHB1 maintains mitochondrial quality in CH. To test this hypothesis, we used Isoproterenol (ISO) to induce CH in H9C2 cells overexpressing PHB1 and elucidated mitochondrial quality control pathways.
Results:
We found that overexpressing PHB1 attenuates ISO-induced CH and restores mitochondrial morphology in H9C2 cells. In addition, PHB1 blocks the pro-hypertrophic IGF1R/AKT pathway and restores the mitochondrial membrane polarization in ISO-treated cells. We observed that overexpressing PHB1 promotes mitochondrial biogenesis, improves mitochondrial respiratory capacity, and triggers mitophagy.
Conclusion:
We conclude that PHB1 maintains mitochondrial quality in ISO-induced CH in H9C2 cells.
Significance:
Based on our results, we suggest that small molecules that induce PHB1 in cardiac cells may prove beneficial in developing cardiac therapies.
More Related Videos
07:40Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
07:14A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
