Abstract
Inflammation is a type of defense response against tissue damage, and can be mediated by lymphocytes and macrophages. Fibrosis is induced by tissue injury and inflammation, which leads to an increase in fibrous connective tissue in organs and a decrease in organ parenchyma cells, finally leading to organ dysfunction or even failure. The vascular niche is composed of endothelial cells, pericytes, macrophages, and hematopoietic stem cells. It forms a guiding microenvironment for the behavior of adjacent cells, and mainly exists in the microcirculation, including capillaries. When an organ is damaged, the vascular niche regulates inflammation and affects the repair of organ damage in a variety of ways, such as via its angiocrine function and transformation of myofibroblasts. In this paper, the main roles of vascular niche in the process of organ fibrosis and its mechanism of promoting the progress of fibrosis through inflammatory immunoregulation are summarized. It was proposed that the vascular niche should be regarded as a new therapeutic target for organ fibrosis, suggesting that antifibrotic effects could be achieved by regulating macrophages, inhibiting endothelial-mesenchymal transition, interfering with the angiocrine function of endothelial cells, and inhibiting the transformation of pericytes into myofibroblasts, thus providing new ideas for antifibrosis drug research.
Highlights
Organ fibrosis comprises an acute or chronic pathological change to organs caused by infection, inflammation, autoimmune reaction, and other factors
We have described the main role of endothelial cells (ECs), pericytes, and macrophages in the vascular niche during fibrosis, which provides us with new directions to find drug targets, such as screening for more single or compound drugs to inhibit organ inflammation and fibrosis according to the molecular mechanisms of the vascular niche
It is feasible to select the vascular niche as a new target for antifibrotic therapy, which can be achieved by inhibiting the endothelial-mesenchymal transition (EndoMT), interfering with the angiocrine function of ECs, inhibiting the transformation of pericytes into myofibroblasts, and regulating macrophages
Summary
Organ fibrosis comprises an acute or chronic pathological change to organs caused by infection, inflammation, autoimmune reaction, and other factors. Fibrosis causes destruction and reduction of parenchymal cells of organs, activation of fibroblasts, production of the extracellular matrix (ECM) (such as collagen, glycoproteins and adhesion proteins), and continuous deposition of ECM on the basement membrane. This results in continuous progress of organ structural disruption, functional decline, and even exhaustion, which seriously threatens human health and life, and is a hot topic in medical research (Budi et al, 2021). The vascular niche is composed of endothelial cells (ECs), pericytes, macrophages, hematopoietic stem cells, adipocytes and nerve cells, and it forms a guiding microenvironment for the behavior of adjacent cells and mainly exists in the microcirculation, including capillaries (Ribatti et al, 2021; Wermuth et al, 2016).
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