TGF-β as A Master Regulator of Aging-Associated Tissue Fibrosis

Fibrosis is the abnormal accumulation of extracellular matrix proteins such as collagen and fibronectin. Aging, injury, infections, and inflammation can cause different types of tissue fibrosis. Numerous clinical investigations have shown a correlation between the degree of liver and pulmonary fibrosis in patients and telomere length and mitochondrial DNA content, both of which are signs of aging. Aging involves the gradual loss of tissue function over time, which results in the loss of homeostasis and, ultimately, an organism's fitness. A major feature of aging is the accumulation of senescent cells. Senescent cells abnormally and continuously accumulate in the late stages of life, contributing to age-related fibrosis and tissue deterioration, among other aging characteristics. Furthermore, aging generates chronic inflammation, which results in fibrosis and decreases organ function. This finding suggests that fibrosis and aging are closely related. The transforming growth factor beta (TGF-beta) superfamily plays a crucial role in the physiological and pathological processes of aging, immune regulation, atherosclerosis, and tissue fibrosis. In this review, the functions of TGF-beta in normal organs, aging, and fibrotic tissues is discussed: TGF-beta signalling is altered with age and is an indicator of pathology associated with tissue fibrosis. In addition, this review discusses the potential targeting of noncoding.

Automated summary

Fibrosis is the accumulation of abnormal extracellular matrix proteins, which can be caused by aging, injury, infections, and inflammation. Telomere length and mitochondrial DNA content, signs of aging, have been correlated with the degree of liver and pulmonary fibrosis in patients. Senescent cells, chronic inflammation, and the role of TGF-beta superfamily in aging and fibrosis are also discussed.