Abstract
The renin-angiotensin system (RAS) regulates diverse cellular responses and is crucial for normal organ development and function. On the other hand, RAS exerts deleterious effects promoting cardiovascular and multiple organ damage and contributes to promoting various aging-related diseases and aging-related decline in multiple organ functions. RAS blockade has been shown to prevent the progression of aging-related phenotypes and promote longevity. Wnt signaling pathway also plays a major role in the regulation of mammalian pathophysiology and is essential for organismal survival, and furthermore, it is substantially involved in the promotion of aging process. In this way, both RAS signaling and Wnt signaling have the functions of antagonistic pleiotropy during the process of growth and aging. Our recent study has demonstrated that an anti-aging effect of RAS blockade is associated with down-regulation of canonical Wnt signaling pathway, providing evidence for the hierarchical relationship between RAS signaling and Wnt signaling in promoting aging-related phenotypes. Here, we review how RAS signaling and Wnt signaling regulate the aging process and promote aging-related diseases.
Highlights
The renin-angiotensin system (RAS) plays pleiotropic roles in regulating mammalian pathophysiology
Angiotensin II (Ang II) type 1 (AT1) receptor is a well-known member of the G proteincoupled receptor family, which shares the structure characterized by seven transmembrane-spanning αhelices
We have demonstrated that serum C1q concentration was increased, and C1q expression and Wnt/β-catenin signaling activity in skeletal muscle were augmented after cryoinjury in mice, but angiotensin II type receptor blocker (ARB) treatment inhibited both the increase in serum C1q level and the activation of C1qWnt/β-catenin signaling in injured muscle [15]
Summary
The renin-angiotensin system (RAS) plays pleiotropic roles in regulating mammalian pathophysiology. We have recently reported that RAS blockade prevented the aging-related functional decline in skeletal muscle and that this anti-aging effect of RAS blockade was associated with down-regulation of Wnt/β-catenin signaling pathway [15]. We have recently reported that AT1a receptor-deficient mice showed less severe aging-related phenotypes in other tissues as well, such as functional decline in skeletal muscle [15]. C1q treatment stimulated fibroblast proliferation and collagen synthesis but suppressed satellite cell proliferation in skeletal muscle, and promoted agingrelated impairment of skeletal muscle regeneration through activation of Wnt/β-catenin signaling [14]. C1q was secreted from macrophages recruited to the aorta in Ang II-infused mice, and C1q-mediated activation of Wnt/β-catenin signaling induced proliferation of vascular smooth muscle cells and promoted arterial remodeling [66]
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