Overview
- Researchers profiled human skeletal muscle from chronic limb‑threatening ischemia patients and mouse limb‑ischemia models and pinpointed the long non‑coding RNA CARMN as reduced in disease tissue.
- CARMN is expressed in vascular smooth muscle cells rather than endothelial cells, shifting attention away from long‑studied endothelial growth factors that have failed in clinical trials.
- Genetic deletion of CARMN in mice produced poor blood‑flow recovery, reduced capillary density, limb tissue necrosis, and amputation‑like outcomes.
- Mechanistic experiments mapped a miR‑143‑3p–HHIP signaling axis controlled by CARMN that links smooth muscle signaling to endothelial angiogenesis and tissue repair.
- Blocking HHIP or elevating its regulating microRNA fully rescued angiogenesis, perfusion, and healing in models, and investigators are now probing upstream regulators that lower CARMN during ischemia.