Despite robust neovascularization, the microcirculation formed by regenerative angiogenesis in skeletal muscle is profoundly flawed in both structure and function, with no evidence for normalizing over time. This network-level dysfunction must be recognized and overcome to advance regenerative approaches for ischemic disease.
The aortic media depends on an intrinsic NAD fueling system to protect against DNA damage and premature SMC senescence, with relevance to human thoracic aortopathy.
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