Key result
Renin-angiotensin system blockade protects against aging-related deleterious effects and promotes longevity through down-regulation of the aging-promoting C1q-Wnt/β-catenin signaling pathway.
The review highlights a hierarchical relationship where RAS blockade exerts anti-aging effects by down-regulating the C1q-Wnt/β-catenin signaling pathway.
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.
No takes yet. Share an insight, caveat, or question.
Kamo et al. (2016) conducted a review in Aging-related phenotypes and diseases. Renin-angiotensin system (RAS) blockade was evaluated. Renin-angiotensin system blockade protects against aging-related deleterious effects and promotes longevity through down-regulation of the aging-promoting C1q-Wnt/β-catenin signaling pathway.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: