Effects of gas signaling molecule SO2 in cardiac functions of hyperthyroid rats

• 발행기관: 대한생리학회-대한약리학회
• 저자명: Qi Yang Ting Yang Xing Liu Shengquan Liu Wei Liu Liangui Nie Chun Chu Jun Yang
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제28권 제2호, 129~143쪽, 전체 15쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2024.03.01

국문 초록

Sulfur dioxide (SO2), a novel endogenous gas signaling molecule, is involved in the regulation of cardiac function. Exerting a key role in progression of hyperthyroidism-induced cardiomyopathy (HTC), myocardial fibrosis is mainly caused by myocardial apoptosis, leading to poor treatment outcomes and progno-ses. This study aimed to investigate the effect of SO2 on the hyperthyroidism-induced myocardial fibrosis and the underlying regulatory mechanisms. Elisa, Masson stain-ing, Western-Blot, transmission electron microscope, and immunofluorescence were employed to evaluate the myocardial interstitial collagen deposition, endoplasmic reticulum stress (ERS), apoptosis, changes in endogenous SO2, and Hippo pathways from in vitro and in vivo experiments. The study results indicated that the hyperthy-roidism-induced myocardial fibrosis was accompanied by decreased cardiac func-tion, and down-regulated ERS, apoptosis, and endogenous SO2-producing enzyme aspartate aminotransferase (AAT)1/2 in cardiac myocytes. In contrast, exogenous SO2 donors improved cardiac function, reduced myocardial interstitial collagen deposi-tion, up-regulated AAT1/2, antagonized ERS and apoptosis, and inhibited excessive activation of Hippo pathway in hyperthyroid rats. In conclusion, the results herein suggested that SO2 inhibited the overactivation of the Hippo pathway, antagonized ERS and apoptosis, and alleviated myocardial fibrosis in hyperthyroid rats. Therefore, this study was expected to identify intervention targets and new strategies for pre-vention and treatment of HTC.

목차

INTRODUCTION

METHODS

RESULTS

DISCUSSION

키워드

Apoptosis Endoplasmic reticulum stress Hippo signaling pathway Hyperthyroidism-induced cardiomyopathy Sulfur dioxide