p38 proteins control a spectrum of processes, and their dysregulation has been linked to various diseases, making them promising pharmacological targets for clinical use.

G protein-coupled receptor kinase 2 (GRK2) has emerged as a pivotal regulator in the pathophysiology of heart failure. GRK2 mediates the phosphorylation of activated G protein‐coupled receptors ...

An often overlooked protein actually a potent regulator of cardiac hypertrophy. ScienceDaily . Retrieved June 3, 2025 from www.sciencedaily.com / releases / 2009 / 11 / 091116143615.htm ...

Heat shock protein 90 (HSP90), one of the most abundant proteins in the cardiac cells is essential for cell survival. Previous studies have shown that angiotensin II induces cardiac cell hypertrophy.

This action by DPF3a leads to an increase in the production of proteins that are normally associated with early cardiac development, and which are typically found in patients with cardiac hypertrophy.

A research team led by Prof. Liu Qingsong from the Hefei Institutes of Physical Science of the Chinese Academy of Science has ...

In this study, we show that pharmacological protein kinase C (PKC) activation induces cardiomyocyte hypertrophy via activation of novel PKC isoforms. Both neonatal rat ventricular cardiomyocytes and ...

When HSPA4 (which is necessary for the maintenance of HSP70) is disrupted, misfolded proteins accumulate in the heart, and spontaneous cardiac hypertrophy develops. 71 Thus, HSPs are necessary for ...

The main mechanisms involved in pathological hypertrophy include inflammatory processes, fibrosis, mitochondrial dysfunction, dysregulation of calcium-handling proteins, metabolic alterations ...

More information: Katharina Dörr et al. Randomized Trial of Etelcalcetide for Cardiac Hypertrophy in Hemodialysis, Circulation Research (2021).DOI: 10.1161/CIRCRESAHA.120.318556 ...

Inhibiting Ca2+ or calmodulin-based protein kinase II (CaMKII) restored pathological APD alterations in female and male HFpEF mice, and empagliflozin treatment matched CaMKII inhibition effects.