Key result
HTR2A promotes cardiac hypertrophy via PI3K-PDK1-AKT-mTOR signaling, whereas its knockdown represses isoproterenol-induced hypertrophy.
Why the study?
The roles of HTR2A in the cardiovascular system, particularly in cardiac hypertrophy, are not fully understood.
Population
Human hypertrophic hearts, ISO-induced cardiac hypertrophy mouse model, neonatal rat cardiomyocytes
Comparison
HTR2A knockdown vs overexpression with or without AKT-mTOR or PI3K/PDK1 inhibition
Design
Preclinical experimental study
Authors
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HTR2A may be a hypertrophy target; leaves open translation from animal models to clinical validation.
HTR2A promotes cardiac hypertrophy by activating the PI3K-PDK1-AKT-mTOR signaling pathway, identifying it as a potential therapeutic target for pathological hypertrophy.
Gao et al. (2020) studied Cardiac hypertrophy. HTR2A knockdown or overexpression was evaluated on Cardiomyocyte hypertrophy. HTR2A promoted cardiac hypertrophy by activating the PI3K-PDK1-AKT-mTOR signaling pathway, whereas its knockdown repressed isoproterenol-induced cardiomyocyte hypertrophy.
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