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

Abstract

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 factorbeta (TGF-β) 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-β in normal organs, aging, and fibrotic tissues is discussed: TGF-β 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.

Innate and Adaptive Immunity-Related Markers as Predictors of the Short-Term Progression of Subclinical Atherosclerosis in Middle-Aged Patients

“…Clinical studies have also confirmed the accumulation of T-regulatory lymphocytes in connection to chronological aging and the association of T-regulatory cells with immunosenescence [41,42]. The expansion of T-regulatory lymphocytes and myeloid derived suppressor cells (MDSC), promotes an increase in TGFβ which is a key regulator of physiological and pathological aging, fibrosis and atherogenesis [43].…”

Trigonelline hydrochloride attenuates silica-induced pulmonary fibrosis by orchestrating fibroblast to myofibroblast differentiation

“…The dysregulation of the TGF-β1/Smad pathway plays an essential role in the pathological process of silicosis [ 44 , 46 ]. TGF-β1 recruits and activates transforming growth factor beta receptor 1(TGFR1) upon binding to TGF-β receptor 2 (TGFβR2).…”

Vasculopathy Augments Cardiovascular Risk in Community-Dwelling Elderly with Left Ventricular Hypertrophy

“…For instance, LVH often results from chronic pressure overload, which can be exacerbated by the arterial stiffness seen in arteriosclerosis and atherosclerosis [ 15 , 16 , 32 ]. Renal senescence might further compound these effects through the interplay of hypertension, dysregulated volume control, and hormonal disturbances affecting cardiovascular health [ 33 , 34 , 35 ]. Clinically, this finding highlights the necessity for a comprehensive approach to managing elderly patients with LVH.…”