Angiogenesis: A Cellular Response to Traumatic Injury

Abstract

The development of new vasculature plays a significant role in a number of chronic disease states, including neoplasm growth, peripheral arterial disease, and coronary artery disease, among many others. Traumatic injury and hemorrhage, however, is an immediate, often dramatic pathophysiologic insult which can also necessitate neovascularization to promote healing.Traditional understanding of angiogenesis involved resident endothelial cells branching outward

Glucose/ROS cascade-responsive ceria nanozymes for diabetic wound healing

“…These results indicated satisfactory hemocompatibility for further biological applications. Then, cytotoxicity tests of CHA@GOx based on HUVECs cells or NIH-3T3 cells were performed, because endothelial cells and fibroblasts play important roles in wound healing [ [57] , [58] , [59] ]. CCK-8 analysis ( Fig.…”

Transcatheter arterial embolization using imipenem/cilastatin sodium and microspheres for traumatic pseudoaneurysm: A case report

“…TAE with IPM/CS may be useful in trauma patients with severe tissue injuries wherein small arteries are involved. Tissue damage induces angiogenesis with rapid capillary growth to supply oxygen and nutrients to the damaged tissue, resulting in increased capillary density [10] . In such cases, small capillaries can form traumatic pseudoaneurysms.…”

An Emerging Frontier in Intercellular Communication: Extracellular Vesicles in Regeneration

“…Proliferation of many types of stem and progenitor cells is required to produce progeny that rebuilds lost and damaged tissue. For example, fibroblast proliferation is required for ECM remodeling ( Plikus et al, 2021 ); endothelial cell proliferation is required to revascularize regenerating tissue ( Pecoraro et al, 2021 ); hepatocytes proliferate to rebuild liver mass ( Chen et al, 2020 ); and multiple cell types proliferate after acute and chronic lung injury ( Kotton and Morrisey, 2014 ). In mammals, injury increases proliferation through a variety of mechanisms, including by stimulating division of tissue-resident stem cell populations ( Hsu and Fuchs, 2021 ); promoting cell cycle re-entry of quiescent stem cells ( Fu et al, 2015 ); activating facultative stem cells that normally exist in a fully differentiated state ( Leach and Morrisey, 2018 ); and expanding rare injury-responsive subpopulations ( Wilson et al, 2008 ; Ayyaz et al, 2019 ).…”

“…For example, fibroblasts migrate to remodel the ECM ( Plikus et al, 2021 ), immune cells extravasate from the blood supply to promote inflammation and clear microbes ( Julier et al, 2017 ), muscle satellite cells migrate to repair damaged muscle ( Choi et al, 2020 ), and MSCs migrate to generate new cartilage, bone, fat, and other tissues ( de Lucas et al, 2018 ). Cells also migrate collectively ( Friedl and Gilmour, 2009 ): epithelial cells migrate in sheets underneath fibrin clots to re-epithelialize cutaneous injuries ( Shaw and Martin, 2009 ), and endothelial cells migrate collectively during angiogenic sprouting and revascularization of new tissue ( Pecoraro et al, 2021 ). Migration is stimulated by environmental cues (e.g., chemokines) as well as mechanical forces, and requires cytoskeletal rearrangements and modulation of cell:cell and cell:matrix interactions ( Trepat et al, 2012 ; Shellard and Mayor, 2020 ).…”