Lee Seung Hyun, Choi Jae-Hoon
Department of Life Science, College of Natural Sciences, Research Institute of Natural Sciences, Hanyang University, Seoul 04763, Korea.
Immune Netw. 2016 Feb;16(1):26-32. doi: 10.4110/in.2016.16.1.26. Epub 2016 Feb 25.
Aortic valve stenosis is a heart disease prevalent in the elderly characterized by valvular calcification, fibrosis, and inflammation, but its exact pathogenesis remains unclear. Previously, aortic valve stenosis was thought to be caused by chronic passive and degenerative changes associated with aging. However, recent studies have demonstrated that atherosclerotic processes and inflammation can induce valvular calcification and bone deposition, leading to valvular stenosis. In particular, the most abundant cell type in cardiac valves, valvular interstitial cells, can differentiate into myofibroblasts and osteoblast-like cells, leading to valvular calcification and stenosis. Differentiation of valvular interstitial cells can be trigged by inflammatory stimuli from several immune cell types, including macrophages, dendritic cells, T cells, B cells, and mast cells. This review indicates that crosstalk between immune cells and valvular interstitial cells plays an important role in the development of aortic valve stenosis.
主动脉瓣狭窄是一种在老年人中普遍存在的心脏病，其特征为瓣膜钙化、纤维化和炎症，但其确切发病机制仍不清楚。以前，主动脉瓣狭窄被认为是由与衰老相关的慢性被动和退行性变化引起的。然而，最近的研究表明，动脉粥样硬化过程和炎症可诱导瓣膜钙化和骨沉积，导致瓣膜狭窄。特别是，心脏瓣膜中最丰富的细胞类型——瓣膜间质细胞，可分化为肌成纤维细胞和成骨样细胞，导致瓣膜钙化和狭窄。瓣膜间质细胞的分化可由几种免疫细胞类型（包括巨噬细胞、树突状细胞、T细胞、B细胞和肥大细胞）的炎性刺激触发。这篇综述表明，免疫细胞与瓣膜间质细胞之间的相互作用在主动脉瓣狭窄的发展中起重要作用。
