Peer-reviewedCC BYCell stress
Glycemia reprograms substrate transport and shapes divergent stress responses in differentiating H9c2 cells
- 1Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy
- 2Department of Life Sciences, University of Siena, Siena, Italy
- 3Department of Molecular and Developmental Medicine, University of Siena, Siena, Italy
Abstract
Metabolic stress is a major determinant of cell fate, particularly during differentiation, when long-lasting adaptations shape cellular responses to subsequent insults. Early-life glycemic instability is increasingly recognized as a stressor capable of programming cardiomyocyte metabolism and vulnerability, yet its direct impact on stress-response pathways during cardiomyocyte differentiation remains poorly defined. Here, we used differentiating H9c2 cardiomyoblasts to model chronic hypoglycemic (2.5 mM), normoglycemic (5 mM), and hyperglycemic (30 mM) conditions as opposing metabolic challenges, and examined their effects on substrate transport, lipid homeostasis, and stress-induced cell death pathways.
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BibTeX
@article{passaponti2026glycemia,
title = {{Glycemia reprograms substrate transport and shapes divergent stress responses in differentiating H9c2 cells}},
author = {Sofia Passaponti and Asia Iserani and Roberta Romagnoli and Laura Cresti and Cinzia Del Gaudio and Alice Luddi and Leonardo Ermini and Francesca Ietta},
journal = {Cell stress},
year = {2026},
month = oct,
doi = {10.15698/cst2026.10.321},
url = {https://europepmc.org/article/PMC/PMC13659450},
note = {CC BY},
}
RIS
TY - JOUR
TI - Glycemia reprograms substrate transport and shapes divergent stress responses in differentiating H9c2 cells
AU - Sofia Passaponti
AU - Asia Iserani
AU - Roberta Romagnoli
AU - Laura Cresti
AU - Cinzia Del Gaudio
AU - Alice Luddi
AU - Leonardo Ermini
AU - Francesca Ietta
PY - 2026
DA - 2026/10/01
JO - Cell stress
DO - 10.15698/cst2026.10.321
UR - https://europepmc.org/article/PMC/PMC13659450
AB - Metabolic stress is a major determinant of cell fate, particularly during differentiation, when long-lasting adaptations shape cellular responses to subsequent insults. Early-life glycemic instability is increasingly recognized as a stressor capable of programming cardiomyocyte metabolism and vulnerability, yet its direct impact on stress-response pathways during cardiomyocyte differentiation remains poorly defined. Here, we used differentiating H9c2 cardiomyoblasts to model chronic hypoglycemic (2.5 mM), normoglycemic (5 mM), and hyperglycemic (30 mM) conditions as opposing metabolic challenges, and examined their effects on substrate transport, lipid homeostasis, and stress-induced cell death pathways.
SN - 2523-0204
ER -