Endocrine Abstracts

Increased body weight and adipose tissue accumulation amplifies the risk of developing various age-related diseases, such as cardiovascular disease, type 2 diabetes mellitus, musculoskeletal disorders. Adipose tissue-derived secreted pro-inflammatory adipokines generate a chronic low-grade inflammation which contributes to the pathogenesis of obesity-linked complications. Recent advancements in tissue-resident adult stem/progenitor cell research have revealed that inflammation, enhanced telomere shortening, oxidative stress, may occur in these immature and regenerative cells during chronological aging. Particularly, the alterations in key signaling components controlling their self-renewal capacity may result in their dysfunctions, growth arrest and senescence or apoptotic death during the aging process. These molecular events may culminate in a progressive decline in the regenerative functions and the number of tissue-resident adult stem/progenitor cells, and age-related disease development. In the microenvironment, inflammation may favor adipose derived stem cell (ASC) differentiation into endothelial cells while inhibiting their differentiation into adipocytes. On the other hand it has been shown that ASCs possess anti-inflammatory properties and promote endothelial cell differentiation and microvascular regeneration.

The chronic low-grade inflammation and oxidative stress cold lead to muscle-to-fat conversion of muscle satellite cells (SCs), thus explaining the increase in intermuscular adipose tissue depots that occurs under some pathological conditions (i.e. primary myodystrophies, obesity, hyperglycaemia, high plasma free fatty acids, hypoxia, age-related sarcopenia, etc.) or simply because of a sedentary lifestyle or during aging. Several pathways and factors (PPARs, WNT growth factors, myokines, GEF-GAP-Rho, p66shc, mitochondrial ROS production, PKCβ) could be implicated in the adipogenic conversion of SCs.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details are unavailable.