id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-012688-d0m23sgk	Zheng, Xu-yong	Compound LM9, a novel MyD88 inhibitor, efficiently mitigates inflammatory responses and fibrosis in obesity-induced cardiomyopathy	2020-04-27		.txt	text/plain	5419	328	55	TLR4/MyD88 signaling pathway, as a key regulator of inflammation, plays an important role in the pathogenesis of obesity-induced cardiomyopathy. We previously demonstrated that LM9, a novel MyD88 inhibitor, attenuated inflammatory responses and fibrosis in obesity-induced cardiomyopathy by inhibiting the formation of TLR4/MyD88 complex. In HFD-fed mice, administration of LM9 (5, 10 mg/kg, ig, every other days for 8 weeks) dose-dependently alleviated inflammation and fibrosis in heart tissues and decreased serum lipid concentration. Thus, in the current study, we provide evidence that compound LM9, a novel MyD88 inhibitor from our previous study [21, 22] , efficiently attenuates inflammatory responses and fibrosis in obesity-induced cardiomyopathy by inhibiting the formation of the TLR4/MyD88 complex. We also examined the expression levels of profibrotic proteins in heart tissue, and our results revealed that LM9 attenuated HFD-induced cardiac fibrosis (Fig. 6d and Supplementary Fig. S1 ). Lipid accumulation activates harmful signaling pathways, resulting in the production of inflammatory factors and tissue remodeling in cardiomyocytes, leading to obesity-induced cardiomyopathy.	./cache/cord-012688-d0m23sgk.txt	./txt/cord-012688-d0m23sgk.txt