The implications of human stem cell differentiation to endothelial cell via fluid shear stress in cardiovascular regenerative medicine: a review.
Stem cell therapy heralds a new chapter in cardiovascular regenerative medicine. Cardiovascular implants are often used in both surgery and interventional cardiology. Cardiovascular stents are utilized in percutaneous coronary interventions (PCI), and are classified as either bare metal stents (BMS) or drug-eluting stents (DES). Although DES might decrease the risk of vascular restenosis, there are complications (e.g. thrombosis) associated with it as well. Many new and novel composite materials are increasingly being developed along the premise of mobilizing and attracting endogenous stem cells to home-in and differentiate into a confluent layer of endothelial cell around the vessel wall. One of the main forces acting on cells in a blood vessel wall is fluid shear stress. Fluid shear stress is vital in establishing the vasculature of the embryo, and different shear stress patterns have been both implicated in maintaining vascular physiology, and also associated with certain pathological conditions. Recent evidence suggests that via a plethora of mechanosensors and mechanotransduction signaling pathways, stem cells differentiate into endothelial cells when exposed to fluid shear stress. Here we review the current knowledge pertaining to the roles that mechanosensors and mechanotransducers play in stem cell differentiation into endothelial cells via fluid shear stress, and its implications for pharmacological applications and cardiovascular implants in the realm of regenerative medicine.
University College London (UCL) Royal Free Hampstead NHS Trust Hospital Pond Street, London NW3 2QG, UK.
Aaron
A
Tan
Bauer E
BE
Sumpio
Samuel
S
Lee
Alexander M
AM
Seifalian
D002318:Cardiovascular Diseases / Q000628:therapy*; D002454:Cell Differentiation; D004730:Endothelium, Vascular / Q000166:cytology*; D006801:Humans; D044968:Regenerative Medicine; D013234:Stem Cells / Q000166:cytology*; D013312:Stress, Physiological