JAK2/STAT3/HMGCS2 signaling aggravates mitochondrial dysfunction and oxidative stress in hyperuricemia-induced cardiac dysfunction

• Published in: Molecular medicine (Cambridge, Mass.) Vol. 31; no. 1; pp. 184 - 23
• Main Authors: Peng, Dewei, He, Xiaoli, Ren, Bowen, Wang, Qian, Peng, Lulu, Jiang, Yue, Huo, Shengqi, Men, Lintong, Shi, Wei, Luo, Pengcheng, Zhu, Mengyin, Zhang, Cuntai, Lv, Jiagao, Lin, Li, Li, Sheng
• Format: Journal Article
• Language: English
• Published: England BioMed Central 13.05.2025; BMC
• Subjects: Animals; Cardiac dysfunction; Disease Models, Animal; Heart Diseases - etiology; Heart Diseases - metabolism; HMGCS2; Hyperuricemia; Hyperuricemia - complications; Hyperuricemia - metabolism; JAK2; Janus Kinase 2 - metabolism; Male; Mice; Mice, Inbred C57BL; Mitochondria - metabolism; Mitochondrial function; Myocytes, Cardiac - metabolism; Oxidative Stress; Signal Transduction; STAT3; STAT3 Transcription Factor - genetics; STAT3 Transcription Factor - metabolism; Uric Acid; Hyperuricemia; HMGCS2; JAK2; Mitochondrial function; Cardiac dysfunction; STAT3

High uric acid levels play a critical role in cardiovascular disease pathophysiology, being closely linked to their occurrence, progression, and prognosis. To enhance prevention and treatment of hyperuricemia-related cardiovascular diseases, understanding underlying mechanisms and identifying novel...