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Download scientific diagram | Interrelationships among Ca 2+ , NO/ONOO 2 and mitochondrial O 2 AE2 in ECs exposed to shear stress (SS or PS) under physiological conditions (top part) or in the context of RP (following ischemia; bottom part). In the top (green) part, although the shear-induced NO increases mitochondrial O 2 AE2 , the mitochondria maintain their function. In the bottom (red) part, both [Ca 2+ ] mt overload and intramitochondrial ONOO 2 contribute to the collapse of DW m resulting in cyt c release and EC apoptosis. Mitochondrial ROS regulate, and are regulated by, [Ca 2+ ] mt , ONOO 2 and DW m. Solid lines indicate activation; broken lines indicate inhibition. (Modified from schematic in Ref. 138). from publication: Fluid Mechanical Forces and Endothelial Mitochondria: A Bioengineering Perspective | Endothelial cell dysfunction is the hallmark of every cardiovascular disease/condition, including atherosclerosis and ischemia/reperfusion injury. Fluid shear stress acting on the vascular endothelium is known to regulate cell homeostasis. Altered hemodynamics is thought to | Shear Stress, Endothelial Dysfunction and Mitochondrial Degradation | ResearchGate, the professional network for scientists.
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