دورية أكاديمية

Supersulfide catabolism participates in maladaptive remodeling of cardiac cells.

التفاصيل البيبلوغرافية
العنوان: Supersulfide catabolism participates in maladaptive remodeling of cardiac cells.
المؤلفون: Zhou L; National Institute for Physiological Sciences, National Institutes of Natural Sciences (NINS), Okazaki, 444-8787, Japan; Exploratory Research Center on Life and Living Systems, NINS, Okazaki, 444-8787, Japan; SOKENDAI (The Graduate University for Advanced Studies), Okazaki, 444-8787, Japan., Nishimura A; National Institute for Physiological Sciences, National Institutes of Natural Sciences (NINS), Okazaki, 444-8787, Japan; Exploratory Research Center on Life and Living Systems, NINS, Okazaki, 444-8787, Japan; SOKENDAI (The Graduate University for Advanced Studies), Okazaki, 444-8787, Japan., Umezawa K; Tokyo Metropolitan Institute for Geriatrics and Gerontology, Tokyo, 173-0015, Japan., Kato Y; Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, 812-8582, Japan., Mi X; Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, 812-8582, Japan., Ito T; National Institute for Physiological Sciences, National Institutes of Natural Sciences (NINS), Okazaki, 444-8787, Japan; Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, 812-8582, Japan., Urano Y; Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo, 113-0033, Japan; Graduate School of Medicine, The University of Tokyo, Tokyo, 113-0033, Japan., Akaike T; Graduate School of Medicine, Tohoku University, Sendai, 980-8575, Japan., Nishida M; National Institute for Physiological Sciences, National Institutes of Natural Sciences (NINS), Okazaki, 444-8787, Japan; Exploratory Research Center on Life and Living Systems, NINS, Okazaki, 444-8787, Japan; SOKENDAI (The Graduate University for Advanced Studies), Okazaki, 444-8787, Japan; Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, 812-8582, Japan. Electronic address: nishida@phar.kyushu-u.ac.jp.
المصدر: Journal of pharmacological sciences [J Pharmacol Sci] 2024 Aug; Vol. 155 (4), pp. 121-130. Date of Electronic Publication: 2024 May 21.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Japanese Pharmacological Society Country of Publication: Japan NLM ID: 101167001 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1347-8648 (Electronic) Linking ISSN: 13478613 NLM ISO Abbreviation: J Pharmacol Sci Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Kyoto, Japan : Japanese Pharmacological Society, c2003-
مواضيع طبية MeSH: Myocytes, Cardiac*/metabolism , Sulfides*/metabolism , Sulfides*/pharmacology , Hydrogen Sulfide*/metabolism , Ventricular Remodeling*, Animals ; Cells, Cultured ; Adenosine Triphosphate/metabolism ; Rats ; Atrophy ; Cardiomegaly/metabolism ; Cardiomegaly/pathology ; Heart Failure/metabolism ; Heart Failure/pathology ; Animals, Newborn ; Rats, Sprague-Dawley
مستخلص: The atrophic myocardium resulting from mechanical unloading and nutritional deprivation is considered crucial as maladaptive remodeling directly associated with heart failure, as well as interstitial fibrosis. Conversely, myocardial hypertrophy resulting from hemodynamic loading is perceived as compensatory stress adaptation. We previously reported the abundant presence of highly redox-active polysulfide molecules, termed supersulfide, with two or more sulfur atoms catenated in normal hearts, and the supersulfide catabolism in pathologic hearts after myocardial infarction correlated with worsened prognosis of heart failure. However, the impact of supersulfide on myocardial remodeling remains unclear. Here, we investigated the involvement of supersulfide metabolism in cardiomyocyte remodeling, using a model of adenosine 5'-triphosphate (ATP) receptor-stimulated atrophy and endothelin-1 receptor-stimulated hypertrophy in neonatal rat cardiomyocytes. Results revealed contrasting changes in intracellular supersulfide and its catabolite, hydrogen sulfide (H 2 S), between cardiomyocyte atrophy and hypertrophy. Stimulation of cardiomyocytes with ATP decreased supersulfide activity, while H 2 S accumulation itself did not affect cardiomyocyte atrophy. This supersulfide catabolism was also involved in myofibroblast formation of neonatal rat cardiac fibroblasts. Thus, unraveling supersulfide metabolism during myocardial remodeling may lead to the development of novel therapeutic strategies to improve heart failure.
Competing Interests: Declaration of competing interest The authors have no conflict of interest.
(Copyright © 2024 The Authors. Production and hosting by Elsevier B.V. All rights reserved.)
فهرسة مساهمة: Keywords: Cardiac remodeling; Fibrosis; Maladaptation; Receptor; Sulfide metabolism
المشرفين على المادة: 0 (Sulfides)
YY9FVM7NSN (Hydrogen Sulfide)
8L70Q75FXE (Adenosine Triphosphate)
9080-49-3 (polysulfide)
تواريخ الأحداث: Date Created: 20240616 Date Completed: 20240616 Latest Revision: 20240616
رمز التحديث: 20240617
DOI: 10.1016/j.jphs.2024.05.002
PMID: 38880546
قاعدة البيانات: MEDLINE
الوصف
تدمد:1347-8648
DOI:10.1016/j.jphs.2024.05.002