Authors: Amira Sabry, Keiko Cawley, Katie Sciuto, Amanda Horiuchi, David Nix, Chris Stubborn, Yukio Saijoh, Alexey V Zaitsev, Junco S Warren
Published: 2019-10-16
DOI: 10.1161/res.125.suppl_1.286
Source: Full article
Our recent study demonstrated that the histone methyltransferase Smyd1 positively regulates cardiac metabolism through transcriptional control of PGC-1α, a key regulator of mitochondrial energetics. However, it is largely unknown whether Smyd1 plays a role in adaptive responses to metabolic stress in cardiomyocytes. Here, we hypothesized that Smyd1 is required for cell survival during metabolic stress through maintaining energetic balance. To address this hypothesis, neonatal rat ventricular myocytes (NRVMs) were cultured in glucose-free media for 24 hours and real-time quantitative PCR was performed. We found that Smyd1 and its downstream target PGC-1α were upregulated during glucose starvation, concurrent with the significant increase of mRNA levels of