Key result
VEGF and EPCs drive ischemic neovascularization but are attenuated by aging, hypercholesterolemia, and diabetes.
Why the study?
Understanding the mechanisms by which organisms maintain tissue viability and restore perfusion during acute or chronic muscle ischemia, along with factors that impair these responses, remains a key area of focus.
This perspective discusses the biological mechanisms, such as biochemical and behavioral splinting, by which organisms adapt to and preserve tissue viability during acute or chronic ischemia.
No takes yet. Share an insight, caveat, or question.
Confirms VEGF centrality in ischemic neovascularization; leaves open clinical translation of adaptive splinting mechanisms.
Jeffrey M. Isner (2000) conducted a review in Tissue ischemia. Endogenous neovascularization in response to tissue ischemia is primarily driven by VEGF and endothelial progenitor cells, a process that can be pathologically attenuated by aging, hypercholesterolemia, and diabetes.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: