PUBLICATION

Pyruvate plus uridine augment mitochondrial respiration and prevent cardiac hypertrophy in zebrafish and H9c2 cells

Authors
Mukherjee, S., Das, S., Das, S., Gupta, S., Hui, S.P., Sengupta, A., Ghosh, A.
ID
ZDB-PUB-250424-15
Date
2025
Source
Journal of Cell Science : (Journal)
Registered Authors
Keywords
Cardiomyocyte hypertrophy, Mitochondria, Phenylephrine, Respiration, Zebrafish
MeSH Terms
none
PubMed
40270134 Full text @ J. Cell Sci.
Abstract
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 on rat neonatal H9c2 cardiomyocytes promotes significant hypertrophy with decreased mitochondrial oxygen consumption rate (OCR), membrane potential, respiratory subunits NDUFB8, UQCRC2, and ATP5a expressions and accumulation of reactive oxygen species (ROS). Surprisingly, 60% reductions in cell survivability were observed in PE-treated cells compared to control cells grown under the respiratory-proficient galactose media. To revert H9c2 hypertrophy and survivability, we performed a screening with compounds that boost mitochondrial OCR and scavenge ROS, and identified pyruvate plus uridine as the best hit. Corroborated with the in vitro study, supplementation of pyruvate plus uridine significantly prevents PE-induced cardiac hypertrophy, pericardial edema, and bradycardia symptoms in zebrafish embryos. Moreover, pyruvate plus uridine decreases the ventricular and atrial area in cardiomyocyte-specific GFP transgenic Tg (myl7:HRAS-EGFP) lines. Using in vitro and in vivo models, we showed that boosting of mitochondrial respiration by pyruvate and scavenging ROS by uridine supplementations conjointly ameliorated cardiac hypertrophy and bradycardia symptoms.
Genes / Markers
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Human Disease / Model
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