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1型强直性肌营养不良的新视野:细胞衰老作为治疗靶点

New Horizons in Myotonic Dystrophy Type 1: Cellular Senescence as a Therapeutic Target.

作者信息

Légaré Cécilia, Berglund J Andrew, Duchesne Elise, Dumont Nicolas A

机构信息

RNA Institute, College of Arts and Sciences, University at Albany-SUNY, Albany, New York, USA.

School of Rehabilitation Sciences, Faculty of Medicine, Université Laval, Quebec, Quebec, Canada.

出版信息

Bioessays. 2025 Mar;47(3):e202400216. doi: 10.1002/bies.202400216. Epub 2024 Dec 26.

Abstract

Myotonic dystrophy type 1 (DM1) is considered a progeroid disease (i.e., causing premature aging). This hypervariable disease affects multiple systems, such as the musculoskeletal, central nervous, gastrointestinal, and others. Despite advances in understanding the underlying pathogenic mechanism of DM1, numerous gaps persist in our understanding, hindering elucidation of the heterogeneity and severity of its symptoms. Accumulating evidence indicates that the toxic intracellular RNA accumulation associated with DM1 triggers cellular senescence. These cells are in a state of irreversible cell cycle arrest and secrete a cocktail of cytokines, referred to as a senescence-associated secretory phenotype (SASP), that can have harmful effects on neighboring cells and more broadly. We hypothesize that cellular senescence contributes to the pathophysiology of DM1, and clearance of senescent cells is a promising therapeutic approach for DM1. We will discuss the therapeutic potential of different senotherapeutic drugs, especially senolytics that eliminate senescent cells, and senomorphics that reduce SASP expression.

摘要

1型强直性肌营养不良症(DM1)被认为是一种早衰性疾病(即导致过早衰老)。这种高度可变的疾病会影响多个系统,如肌肉骨骼系统、中枢神经系统、胃肠道等。尽管在理解DM1潜在致病机制方面取得了进展,但我们的认识仍存在许多空白,这阻碍了对其症状异质性和严重程度的阐明。越来越多的证据表明,与DM1相关的有毒细胞内RNA积累会引发细胞衰老。这些细胞处于不可逆的细胞周期停滞状态,并分泌一系列细胞因子,称为衰老相关分泌表型(SASP),其可对邻近细胞及更广泛的细胞产生有害影响。我们假设细胞衰老促成了DM1的病理生理学,清除衰老细胞是一种有前景的DM1治疗方法。我们将讨论不同衰老治疗药物的治疗潜力,尤其是消除衰老细胞的衰老溶解剂和降低SASP表达的衰老形态调节剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/08d0/11848125/e1349239ca5b/BIES-47-e202400216-g001.jpg

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