Effect of aging on cellular mechanotransduction

Abstract

Aging is becoming a critical heath care issue and a burgeoning economic burden on society. Mechanotransduction is the ability of the cell to sense, process, and respond to mechanical stimuli and is an important regulator of physiologic function that has been found to play a role in regulating gene expression, protein synthesis, cell differentiation, tissue growth, and most recently, the pathophysiology of disease. Here we will review some of the recent findings of this field and attempt, where possible, to present changes in mechanotransduction that are associated with the aging process in several selected physiological systems, including musculoskeletal, cardiovascular, neuronal, respiratory systems and skin.

Effects of resistive exercise and stretching on the soleus muscle of ovariectomized rats

“…This outcome suggests that the overload due to the body weight, associated with the load to perform resistive exercise, should have induced sarcomerogenesis. According to Wu et al 25 mechanical loading and contractile activity play critical roles in the regulation of muscle mass and altered loading can lead to the structural remodeling of skeletal muscle.…”

The Mechanobiology of Aging

“…In vitro studies conducted to measure the motility as a function of age of fibroblast cells plated on flat substrates have indicated that there is a decrease in overall single-cell translocation with age (31). Wound healing in elderly individuals is hampered (32) by a cohort of factors including a decreased capacity to produce ECM components, such as collagens and elastins; increased collagen fragmentation; increased MMPs; reduced collagen solubility and increased fibrosis; a reduced rate of HIF-1α (hypoxia-inducible factor-1α) mRNA and HIF-1α production (33), which influence ECM production (2, 34); a decreased sensitivity to chemotactic and mechanical stimulation (35); reduced motility and translocation by single cells and clusters of cells (31, 34); a reduced proliferation and number of fibroblasts in older tissue; an increased ratio of senescent to normal cells (20); enhanced ROS (1); depleted adenosine triphosphate (ATP) generation (11); and reduced epithelialization (29). …”

Gαq/11-mediated intracellular calcium responses to retrograde flow in endothelial cells

“…shear stress; endothelium; G protein-␣; inositol 1,4,5-trisphosphate receptor DISTURBED LAMINAR shear stress patterns, including retrograde flow, are known promoters of atherogenic signaling. These variations of hemodynamic parameters may occur naturally as a result of an increased vascular tone in the downstream resistant vessel beds, the geometrical nature of the vessels (anatomical curvature), or by the increase in diastolic retrograde flow often exacerbated with aging, hypertension, or obesity (40). It was recently shown that even at rest, older subjects exhibit greater brachial retrograde flow compared with younger subjects (30).…”