FAM19A5 in vascular aging and osteoporosis: Mechanisms and the "calcification paradox"

被引:0
|
作者
Zheng, Jin [1 ]
He, Jieyu [2 ]
Li, Huahua [1 ,3 ]
机构
[1] Hunan Normal Univ, Hunan Prov Peoples Hosp, Dept Geriatr, Affiliated Hosp 1, Changsha, Hunan, Peoples R China
[2] Cent South Univ, Xiangya Hosp 2, Dept Geriatr, Changsha, Hunan, Peoples R China
[3] Hunan Normal Univ, Hunan Prov People symbolscript Hosp, Dept Geriatr, Affiliated Hosp 1, Changsha 410005, Hunan, Peoples R China
关键词
Vascular aging; Vascular smooth muscle cells; Osteoporosis; Tumor; SMOOTH-MUSCLE-CELLS; BONE-MINERAL DENSITY; KAPPA-B LIGAND; RECEPTOR ACTIVATOR; OXIDATIVE STRESS; ENDOTHELIAL DYSFUNCTION; NEUROVASCULAR UNIT; RANKL; EXPRESSION; OSTEOPROTEGERIN;
D O I
10.1016/j.arr.2024.102361
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Aging induces a progressive decline in the vasculature's structure and function. Vascular aging is a determinant factor for vascular ailments in the elderly. FAM19A5, a recently identified adipokine, has demonstrated involvement in multiple vascular aging-related pathologies, including atherosclerosis, cardio-cerebral vascular diseases and cognitive deficits. This review summarizes the current understanding of FAM19A5' role and explores its putative regulatory mechanisms in various aging-related disorders, including cardiovascular diseases (CVDs), metabolic diseases, neurodegenerative diseases and malignancies. Importantly, we provide novel insights into the underlying therapeutic value of FAM19A5 in osteoporosis. Finally, we outline future perspectives on the diagnostic and therapeutic potential of FAM19A5 in vascular aging-related diseases.
引用
收藏
页数:11
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