Panel A: A diagram showing how mechanical stress affects barrier tissues such as the lungs, gut, and skin. The lungs are depicted with cyclic pressure and stretch due to breathing, the gut with shear stress and luminal pressure, and the skin with friction and compression. Pathological conditions like assisted ventilation, asthmatic bronchoconstriction, obstruction, dysmotility, cellular overcrowding, and excessive tension are mentioned. Panel B: A diagram comparing healthy young stroma, fibrotic stroma, and aged stroma. Healthy stroma shows controlled extracellular matrix (ECM) turnover and homeostatic immune surveillance. Fibrotic stroma depicts excess ECM deposition, collagen crosslinking, myofibroblast activation, and pro-fibrotic inflammation. Aged stroma shows impaired ECM turnover, collagen fragmentation, fibroblast senescence, and inflammaging. Panel C: A diagram illustrating the effects of hemodynamic forces on vascular inflammation. Atheroprotective laminar flow and normal blood pressure maintain endothelial homeostasis, while atherogenic disturbed flow and hypertension promote endothelial activation, atherosclerotic plaque formation, and monocyte recruitment.
Mechanical regulation of inflammatory responses across tissues. (A) Barrier tissues such as the lungs, gut, and skin are constantly exposed to mechanical stress, including stretch, pressure, and shear, which shape epithelial and immune homeostasis. (B) In healthy young stroma, controlled ECM turnover supports physiological force transmission and immune surveillance, whereas fibrosis and aging drive pathological ECM remodeling, increased tissue stiffness, and altered mechanotransduction that amplify inflammatory signaling. (C) Vascular inflammation is modulated by hemodynamic forces, with laminar flow and normal blood pressure maintaining endothelial homeostasis, while disturbed flow and hypertension promote endothelial dysfunction and accelerate atherosclerotic plaque development.