Lactate regulates pathological cardiac hypertrophy via histone lactylation modification

Under the long‐term pressure overload stimulation, the heart experiences embryonic gene activation, leading to myocardial hypertrophy and ventricular remodelling, which can ultimately result in the development of heart failure. Identifying effective therapeutic targets is crucial for the prevention...

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Veröffentlicht in:	Journal of cellular and molecular medicine Jg. 28; H. 16; S. e70022 - n/a
Hauptverfasser:	Zhao, Shuai‐Shuai, Liu, Jinlong, Wu, Qi‐Cai, Zhou, Xue‐Liang
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	England John Wiley & Sons, Inc 01.08.2024 John Wiley and Sons Inc
Schlagworte:	Angiotensin II Animal models Animals Antibodies Cardiac function cardiac hypertrophy Cardiomegaly - metabolism Cardiomegaly - pathology Cardiomyocytes Carotid arteries Cell growth Collagen Congestive heart failure Disease Models, Animal Embryogenesis Environmental effects Epigenetics Gene expression Genetic variability Glucose Glucose - metabolism Glycolysis H3K18la Heart histone lysine lactylation Histones Histones - metabolism HKla Hypertrophy Hypoxia Ischemia Lactic acid Lactic Acid - metabolism Lysine - metabolism Male Metabolism Mice Mice, Inbred C57BL Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Neonates Original Ostomy Phosphorylation post‐translational modification Protein Processing, Post-Translational Surgery Therapeutic targets Veins & arteries United States > US China HKla H3K18la cardiac hypertrophy histone lysine lactylation post‐translational modification
ISSN:	1582-1838, 1582-4934, 1582-4934
Online-Zugang:	Volltext
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