Adipose tissue in older individuals: a contributing factor to sarcopenia

肌萎缩 脂肪组织 医学 老年学 内科学
作者
Tiantian Wang,Dongmei Zhou,Zhen Hong
出处
期刊:Metabolism-clinical and Experimental [Elsevier]
卷期号:160: 155998-155998 被引量:1
标识
DOI:10.1016/j.metabol.2024.155998
摘要

Sarcopenia is a geriatric syndrome characterized by a functional decline in muscle. The prevalence of sarcopenia increases with natural aging, becoming a serious health problem among elderly individuals. Therefore, understanding the pathology of sarcopenia is critical for inhibiting age-related alterations and promoting health and longevity in elderly individuals. The development of sarcopenia may be influenced by interactions between visceral and subcutaneous adipose tissue and skeletal muscle, particularly under conditions of chronic low-grade inflammation and metabolic dysfunction. This hypothesis is supported by the following observations: (i) accumulation of senescent cells in both adipose tissue and skeletal muscle with age; (ii) gut dysbiosis, characterized by an imbalance in gut microbial communities as the main trigger for inflammation, sarcopenia, and aged adipose tissue; and (iii) microbial dysbiosis, which could impact the onset or progression of a senescent state. Moreover, adipose tissue acts as an endocrine organ, releasing molecules that participate in intricate communication networks between organs. Our discussion focuses on novel adipokines and their role in regulating adipose tissue and muscle, particularly those influenced by aging and obesity, emphasizing their contributions to disease development. On the basis of these findings, we propose that age-related adipose tissue and sarcopenia are disorders characterized by chronic inflammation and metabolic dysregulation. Finally, we explore new potential therapeutic strategies involving specialized proresolving mediator (SPM) G protein-coupled receptor (GPCR) agonists, non-SPM GPCR agonists, transient receptor potential (TRP) channels, antidiabetic drugs in conjunction with probiotics and prebiotics, and compounds designed to target senescent cells and mitigate their pro-inflammatory activity.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
大幅提高文件上传限制,最高150M (2024-4-1)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
感动的芝麻完成签到,获得积分10
刚刚
1秒前
ding应助顺心的水之采纳,获得10
2秒前
雪生在无人荒野完成签到,获得积分10
3秒前
4秒前
单纯糖豆发布了新的文献求助10
5秒前
qingxu完成签到,获得积分20
7秒前
SXYYXS发布了新的文献求助10
8秒前
11秒前
Young完成签到,获得积分10
11秒前
不配.应助shaco采纳,获得10
11秒前
白河完成签到,获得积分10
13秒前
14秒前
Ava应助suijisuiji1采纳,获得10
15秒前
善学以致用应助单纯糖豆采纳,获得10
15秒前
白河发布了新的文献求助10
17秒前
Lucas应助无奈柚子采纳,获得10
17秒前
w8816完成签到,获得积分10
18秒前
glowworm完成签到 ,获得积分10
19秒前
ZJ-195发布了新的文献求助10
20秒前
24秒前
慕青应助hcq采纳,获得10
25秒前
可乐不加冰完成签到,获得积分10
27秒前
善学以致用应助夏青荷采纳,获得10
29秒前
passion完成签到,获得积分10
29秒前
30秒前
小小果妈发布了新的文献求助10
31秒前
开朗黑猫完成签到,获得积分10
33秒前
无奈柚子发布了新的文献求助10
33秒前
33秒前
Lucas应助太清采纳,获得10
34秒前
Zjin宇完成签到,获得积分10
35秒前
35秒前
不配.应助shaco采纳,获得10
35秒前
Owen应助小小果妈采纳,获得10
38秒前
李嶍烨发布了新的文献求助10
39秒前
hcq发布了新的文献求助10
39秒前
39秒前
whuhustwit发布了新的文献求助10
39秒前
无奈柚子完成签到,获得积分10
40秒前
高分求助中
Sustainability in Tides Chemistry 2800
The Young builders of New china : the visit of the delegation of the WFDY to the Chinese People's Republic 1000
Rechtsphilosophie 1000
Bayesian Models of Cognition:Reverse Engineering the Mind 888
Le dégorgement réflexe des Acridiens 800
Defense against predation 800
Very-high-order BVD Schemes Using β-variable THINC Method 568
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3136151
求助须知:如何正确求助?哪些是违规求助? 2787065
关于积分的说明 7780419
捐赠科研通 2443217
什么是DOI,文献DOI怎么找? 1298945
科研通“疑难数据库(出版商)”最低求助积分说明 625294
版权声明 600870