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Serpina3c 在生理和病理过程中的多功能作用:对近期研究的综述。

The versatile role of Serpina3c in physiological and pathological processes: a review of recent studies.

机构信息

School of Exercise and Health and Shanghai Frontiers Science Research Base of Exercise and Metabolic Health, Shanghai University of Sport, Shanghai, China.

出版信息

Front Endocrinol (Lausanne). 2023 May 23;14:1189007. doi: 10.3389/fendo.2023.1189007. eCollection 2023.

DOI:10.3389/fendo.2023.1189007
PMID:37288300
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10242157/
Abstract

Murine Serpina3c belongs to the family of serine protease inhibitors (Serpins), clade "A" and its human homologue is SerpinA3. Serpina3c is involved in some physiological processes, including insulin secretion and adipogenesis. In the pathophysiological process, the deletion of Serpina3c leads to more severe metabolic disorders, such as aggravated non-alcoholic fatty liver disease (NAFLD), insulin resistance and obesity. In addition, Serpina3c can improve atherosclerosis and regulate cardiac remodeling after myocardial infarction. Many of these processes are directly or indirectly mediated by its inhibition of serine protease activity. Although its function has not been fully revealed, recent studies have shown its potential research value. Here, we aimed to summarize recent studies to provide a clearer view of the biological roles and the underlying mechanisms of Serpina3c.

摘要

鼠源 Serpina3c 属于丝氨酸蛋白酶抑制剂(Serpins)家族“A”簇,其人类同源物是 SerpinA3。Serpina3c 参与了一些生理过程,包括胰岛素分泌和脂肪生成。在病理生理过程中,Serpina3c 的缺失导致更严重的代谢紊乱,如非酒精性脂肪肝(NAFLD)加重、胰岛素抵抗和肥胖。此外,Serpina3c 可以改善动脉粥样硬化,并调节心肌梗死后的心脏重塑。这些过程中的许多都是直接或间接通过其对丝氨酸蛋白酶活性的抑制来介导的。尽管其功能尚未完全揭示,但最近的研究表明了它具有潜在的研究价值。在这里,我们旨在总结最近的研究,以更清楚地了解 Serpina3c 的生物学作用和潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/fc9be225fae0/fendo-14-1189007-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/d7c44dbe19b7/fendo-14-1189007-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/1d13023907c0/fendo-14-1189007-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/df20ac35283d/fendo-14-1189007-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/55d1096b6863/fendo-14-1189007-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/63cb726b90c0/fendo-14-1189007-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/89b946a5fba0/fendo-14-1189007-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/fc9be225fae0/fendo-14-1189007-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/d7c44dbe19b7/fendo-14-1189007-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/1d13023907c0/fendo-14-1189007-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/df20ac35283d/fendo-14-1189007-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/55d1096b6863/fendo-14-1189007-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/63cb726b90c0/fendo-14-1189007-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/89b946a5fba0/fendo-14-1189007-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d2ae/10242157/fc9be225fae0/fendo-14-1189007-g007.jpg

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