Uploaded May 2025 | Updated September 2026, 3 weeks ago
At The Company of Biologists, we’re always looking for new ways to promote the research published in our journals. We have therefore introduced 'JCS snapshots' where we invite the authors of recently published articles to produce short videos to cover the main findings in their research.
In this video, Alok Ghosh presents their research examining the role of mitochondrial respiration in cardiomyocyte hypertrophy. This research was published in our ‘Cell biology of mitochondria’ special issue, which was coordinated by self-confessed ‘mitochondriaks’ Ana Garcia-Saez and Heidi McBride. You can read their Editorial here: journals.biologists.com/jcs/article/138/9/jcs264067/367979/Special-Issue-Cell-Biology-of-Mitochondria.
Full article: journals.biologists.com/jcs/article/138/9/jcs263653/367983/Pyruvate-plus-uridine-augments-mitochondrial
Pyruvate plus uridine augments mitochondrial respiration and prevents cardiac hypertrophy in zebrafish and H9c2 cells
Soumyajit Mukherjee, Shreya Das, Surajit Das, Samudra Gupta, Subhra Prakash Hui, Arunima Sengupta, Alok Ghosh
Dysfunction of mitochondrial pyruvate oxidation and aberrant respiratory chain components are common in cardiac defects. However, the precise role of mitochondrial respiration in cardiomyocyte hypertrophy is unclear. Phenylephrine (PE) treatment of rat neonatal H9c2 cardiomyocytes promotes significant hypertrophy with decreased mitochondrial oxygen consumption rate (OCR), membrane potential, respiratory subunit NDUFB8, UQCRC2 and ATP5A (ATP5F1A) expression, and accumulation of reactive oxygen species (ROS). Surprisingly, a 60% reduction in cell survival was observed in PE-treated cells relative to control cells when grown under the respiratory-proficient galactose medium. To revert H9c2 hypertrophy and increase survival, we performed a screening with compounds that boost mitochondrial OCR and scavenge ROS, and identified pyruvate plus uridine as the best hit. As corroboration of the in vitro study, supplementation of pyruvate plus uridine significantly prevented PE-induced cardiac hypertrophy, pericardial edema and bradycardia symptoms in zebrafish embryos. Moreover, pyruvate plus uridine decreased the ventricular and atrial area in cardiomyocyte-specific GFP transgenic Tg (myl7:HRAS-EGFP) lines. Using in vitro and in vivo models, we show that boosting of mitochondrial respiration through pyruvate supplementation and scavenging ROS through uridine supplementation jointly ameliorate cardiac hypertrophy and bradycardia symptoms.
At The Company of Biologists, we’re always looking for new ways to promote the research published in our journals. We have therefore introduced 'JCS snapshots' where we invite the authors of recently published articles to produce short videos to cover the main findings in their research.
In this video, Alok Ghosh presents their research examining the role of mitochondrial respiration in cardiomyocyte hypertrophy. This research was published in our ‘Cell biology of mitochondria’ special issue, which was coordinated by self-confessed ‘mitochondriaks’ Ana Garcia-Saez and Heidi McBride. You can read their Editorial here: journals.biologists.com/jcs/article/138/9/jcs264067/367979/Special-Issue-Cell-Biology-of-Mitochondria.
Full article: journals.biologists.com/jcs/article/138/9/jcs263653/367983/Pyruvate-plus-uridine-augments-mitochondrial
Pyruvate plus uridine augments mitochondrial respiration and prevents cardiac hypertrophy in zebrafish and H9c2 cells
Soumyajit Mukherjee, Shreya Das, Surajit Das, Samudra Gupta, Subhra Prakash Hui, Arunima Sengupta, Alok Ghosh
Dysfunction of mitochondrial pyruvate oxidation and aberrant respiratory chain components are common in cardiac defects. However, the precise role of mitochondrial respiration in cardiomyocyte hypertrophy is unclear. Phenylephrine (PE) treatment of rat neonatal H9c2 cardiomyocytes promotes significant hypertrophy with decreased mitochondrial oxygen consumption rate (OCR), membrane potential, respiratory subunit NDUFB8, UQCRC2 and ATP5A (ATP5F1A) expression, and accumulation of reactive oxygen species (ROS). Surprisingly, a 60% reduction in cell survival was observed in PE-treated cells relative to control cells when grown under the respiratory-proficient galactose medium. To revert H9c2 hypertrophy and increase survival, we performed a screening with compounds that boost mitochondrial OCR and scavenge ROS, and identified pyruvate plus uridine as the best hit. As corroboration of the in vitro study, supplementation of pyruvate plus uridine significantly prevented PE-induced cardiac hypertrophy, pericardial edema and bradycardia symptoms in zebrafish embryos. Moreover, pyruvate plus uridine decreased the ventricular and atrial area in cardiomyocyte-specific GFP transgenic Tg (myl7:HRAS-EGFP) lines. Using in vitro and in vivo models, we show that boosting of mitochondrial respiration through pyruvate supplementation and scavenging ROS through uridine supplementation jointly ameliorate cardiac hypertrophy and bradycardia symptoms.
