A circular RNA, circKif26b, declines in aged endothelial tissue, and its loss tracks with reduced capacity to form new blood vessels. Restoring circKif26b stabilized the scaffold protein MOB4 and suppressed Hippo pathway signaling, recovering angiogenic function in aged models. Vascular repair capacity is a rate-limiting factor in tissue perfusion, wound healing, and organ resilience across the lifespan.
Key Points
- circKif26b declines with age, impairing new blood vessel formation
- Restoring circKif26b stabilizes MOB4 and suppresses Hippo signaling
- Angiogenic capacity recovered in aged preclinical vascular models
Longevity Analysis
Perfusion underwrites nearly every repair process in the body; when capillary networks fail to extend into tissue under demand, healing slows, oxygen delivery falls, and functional decline follows in muscle, brain, and skin alike. Identifying a specific regulatory RNA upstream of the Hippo pathway gives a molecular reading of why aged vasculature stops responding to growth signals rather than simply documenting that it does. Practically, this reinforces the value of interventions that place genuine demand on the vascular bed — sustained aerobic work, heat and cold exposure, blood flow restriction — since the machinery of vessel growth remains intact in aged tissue and appears to be signal-limited rather than permanently lost.
Original published by Nature - npj Aging, by Rencong Chen.