Nerve injury–induced protein 1 (Ninjurin 1) is a cell surface adhesion molecule that contains one extracellular adhesion domain and two transmembrane domains. Originally discovered in nerve injury, it has been extensively studied for its role in nerve regeneration. Ninj1 mediates the transendothelial migration of myeloid cells mainly through the extracellular adhesion domain, thereby aggravating the inflammation of the central nervous system. In addition to regulating the inflammatory phenotype of cells, Ninj1 actively mediates the rupture of the plasma membrane and regulates the programmed death of inflammatory cells, thereby participating in the host defense against exogenous infection. In recent years, Ninj1, an important protein associated with inflammasome activation, has garnered increasing attention from researchers regarding its mechanistic role and pathophysiological significance in cardiovascular diseases. Accumulating evidence suggests that Ninj1 not only participates in the regulation of inflammatory responses and cell death processes but also plays a critical role in the onset and progression of various cardiovascular conditions, including atherosclerosis, myocardial ischemia–reperfusion injury, and heart failure. Therefore, an in‐depth exploration of the specific functions of Ninj1 in the cardiovascular system holds significant scientific and clinical value for elucidating the molecular mechanisms underlying these diseases and for developing novel therapeutic strategies. This review aims to summarize the research progress on Ninj1 in cardiovascular diseases and to outline its mechanisms in pathological processes.
Xu et al. (Thu,) studied this question.