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探索炎症性衰老与细胞衰老在机体衰老和疾病中的新兴双向关联。

Exploring the emerging bidirectional association between inflamm-aging and cellular senescence in organismal aging and disease.

机构信息

Nutrigerontology Laboratory, Faculty of Applied Sciences and Biotechnology, Shoolini University, Solan, India.

出版信息

Cell Biochem Funct. 2024 Mar;42(2):e3970. doi: 10.1002/cbf.3970.

DOI:10.1002/cbf.3970
PMID:38456500
Abstract

There is strong evidence that most individuals in the elderly population are characterized by inflamm-aging which refers to a subtle increase in the systemic pro-inflammatory environment and impaired innate immune activation. Although a variety of distinct factors are associated with the progression of inflamm-aging, emerging research is demonstrating a dynamic relationship between the processes of cellular senescence and inflamm-aging. Cellular senescence is a recognized factor governing organismal aging, and through a characteristic secretome, accumulating senescent cells can induce and augment a pro-inflammatory tissue environment that provides a rationale for immune system-independent activation of inflamm-aging and associated diseases. There is also accumulating evidence that inflamm-aging or its components can directly accelerate the development of senescent cells and ultimately senescent cell burden in tissues in a likely vicious inflammatory loop. The present review is intended to describe the emerging senescence-based molecular etiology of inflamm-aging as well as the dynamic reciprocal interactions between inflamm-aging and cellular senescence. Therapeutic interventions concurrently targeting cellular senescence and inflamm-aging are discussed and limitations as well as research opportunities have been deliberated. An effort has been made to provide a rationale for integrating inflamm-aging with cellular senescence both as an underlying cause and therapeutic target for further studies.

摘要

有强有力的证据表明,老年人群体中的大多数人都表现出炎症衰老的特征,这是指全身促炎环境的轻微增加和固有免疫激活受损。尽管许多不同的因素与炎症衰老的进展有关,但新的研究正在证明细胞衰老和炎症衰老之间的动态关系。细胞衰老被认为是控制生物体衰老的一个因素,通过特征性的分泌组,积累的衰老细胞可以诱导和增强促炎的组织环境,为免疫系统独立激活炎症衰老和相关疾病提供了合理依据。越来越多的证据表明,炎症衰老或其成分可以直接加速衰老细胞的发展,并最终导致组织中衰老细胞负担的增加,形成一个可能的恶性循环炎症环路。本综述旨在描述炎症衰老的新兴基于衰老的分子病因学,以及炎症衰老和细胞衰老之间的动态相互作用。讨论了同时针对细胞衰老和炎症衰老的治疗干预措施,并审议了其局限性和研究机会。我们努力为将炎症衰老与细胞衰老结合起来作为进一步研究的潜在原因和治疗靶点提供依据。

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Cell Biochem Funct. 2024 Mar;42(2):e3970. doi: 10.1002/cbf.3970.
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