Contribution of cell death signaling to blood vessel formation

Abstract

The formation of new blood vessels is driven by proliferation of endothelial cells (ECs), elongation of maturing vessel sprouts and ultimately vessel remodeling to create a hierarchically structured vascular system. Vessel regression is an essential process to remove redundant vessel branches in order to adapt the final vessel density to the demands of the surrounding tissue. How exactly vessel regression occurs and whether and to which extent cell death contributes to this process has been in the focus of several studies within the last decade. On top, recent findings challenge our simplistic view of the cell death signaling machinery as a sole executer of cellular demise, as emerging evidences suggest that some of the classic cell death regulators even promote blood vessel formation. This review summarizes our current knowledge on the role of the cell death signaling machinery with a focus on the apoptosis and necroptosis signaling pathways during blood vessel formation in development and pathology.

Klotho promotes AMPK activity and maintains renal vascular integrity by regulating the YAP signaling pathway

“…Blood vessels are a very important organ for mammals, the role of which is to distribute nutrients and oxygen to the whole body under the action of the heart pump, collect waste through the action of the heart pump, and complete the exchange in the lung and liver [1][2][3][4][5]. Blood vessels can be divided into arteries, veins, and capillaries.…”

“…Blood vessels can be divided into arteries, veins, and capillaries. Except for capillaries, which are lined by a single layer of cells, the vascular wall of arteries and veins can be divided into three layers, including the outer membrane (composed of loose connective tissue, elastic fibers, and collagen fibers [1][2][3][4][5]; it is the boundary layer between the blood Ivyspring International Publisher vessel wall and tissue), middle membrane (composed of the basement membrane, microfibrils, collagen, smooth muscle, and elastic fibers; it supports, coagulates, and participates in the relaxation and contraction of blood vessels), and inner membrane (composed of a single layer of vascular endothelial cells, which release a variety of vascular factors and plasminogen). Vascular endothelial cells (ECs) play a very important role in the development, formation, and maintenance of blood vessels [6,7].…”

In situphoto-crosslinked adhesive hydrogel loaded with mesenchymal stem cell-derived extracellular vesicles promotes diabetic wound healing

“…In the stage of remodelling, the neovessels transform into less dense but well-perfused blood vessels via vessel pruning. 55,56 TGF-β is deemed a double-edged sword in the wound healing process. The functional activation of fibroblasts and keratinocytes, the primary cell types in skin repair, is associated with increased expression of TGF-β.…”

YTHDF2-mediated Distinct m6A Regulations Bifurcate Ferroptosis and Apoptosis in BHPF-induced Developmental Defects

“…2a), implying the involvement of cell death. Considering the close relationship between programmed cell death and cardiac injury [29][30][31][32] , we screened the main programmed cell death inhibitors for their protective effects on BHPF-induced cardiotoxicity. Only the ferroptosis inhibitor Ferrostatin-1 (Fer-1) showed cardioprotective effects, with a rebound in zebrafish heart rate (Fig.…”