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http://dx.doi.org/10.1113/JP272680 | DOI Listing |
Int Heart J
September 2025
Department of Cardiovascular Medicine, Tokushima University Graduate School of Biomedical Sciences.
The pharmacological blockade of mineralocorticoid receptors (MR) is a potential therapeutic approach to reduce cardiovascular complications. Recent studies suggest that MR blockers affect several extrarenal tissues, including vascular function. We investigated the effects of a novel non-steroidal selective MR blocker, esaxerenone, on vascular function and atherogenesis.
View Article and Find Full Text PDFBiochem Biophys Res Commun
September 2025
King's College London, GKT School of Medical Education, London, UK. Electronic address:
Heart failure remains a major global health concern characterized by complex pathophysiological processes and significant clinical challenges. While the distinct roles of metabolic and epigenetic dysregulation in heart failure are increasingly recognized, their intricate interplay remains a critical, yet underexplored, aspect of its pathophysiology. This review provides a comprehensive examination of this metabolic-epigenetic crosstalk, exploring how metabolic changes, such as impaired fatty acid oxidation, increased glycolysis, and mitochondrial dysfunction, alter epigenetic landscapes through shifts in intermediary metabolites including acetyl-CoA, NAD+, and α-ketoglutarate.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
September 2025
Department of Medical Pharmacology and Physiology, School of Medicine, University of Missouri.
The sarcomeric protein cardiac myosin binding protein-C (cMyBP-C) binds myosin on thick filaments and regulates cardiac myocyte contraction. Our lab has reported that permeabilized cardiac myocytes lacking cMyBP-C generate greater power and show disproportionately fast sarcomere shortening velocities at high loads. Also, high resolution X-ray diffraction of cardiac trabeculae found that myosin cross-bridges in the cMyBP-C zone are the most active during loaded contractions.
View Article and Find Full Text PDFRev Cardiovasc Med
August 2025
Department of Cardiovascular Medicine, Third Hospital of Shanxi Medical University, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, 030032 Taiyuan, Shanxi, China.
The AMP-activated protein kinase (AMPK) alpha (AMPK) subunit is the catalytic subunit in the AMPK complex and includes both 1 and 2 isoforms. Phosphorylation of upstream kinases at the Thr172 site in the -subunit is critical for AMPK activation. The kinases upstream of AMPK include liver kinase B1 (LKB1), calcium/calmodulin-dependent protein kinase kinase (CaMKK), and transforming growth factor -activated kinase 1 (TAK1).
View Article and Find Full Text PDFJCI Insight
September 2025
Department of Pharmacology, University of Michigan, Ann Arbor, United States of America.
Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure. We examined how S-palmitoylation of the small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), impacts cardiomyocyte stress signaling. Mutation of the cysteine-178 palmitoylation site impaired activation of Rac1 when overexpressed in cardiomyocytes.
View Article and Find Full Text PDF