A comprehensive microRNA expression and function landscape of human wounds unraveled miRNAs highly relevant to venous ulcer pathology.

After an injury to the skin, murine wounds upregulate apoptosis and efferocytosis pathways, which are required for effective healing and may similarly impact wound healing in diabetic patients.

The targeted removal of legacy bisphosphonate from the jawbone by competitive equilibrium therapy not only elucidated the pathological mechanism of bisphosphonate-related osteonecrosis of the jaw (BRONJ) but also established a highly translatable therapeutic option for BRONJ.

Enterococcus faecalis infection elicits a cellular response marked by novel bacterial-host interactions, revealing insights into immune evasion mechanisms in chronic wound infections.

Therapeutic potential of CCL3 for the treatment of diabetic foot ulcers if it is applied topically after the surgical debridement.

A small molecule compound Dwn1, identified through high-throughput screening using Npas2 as the molecular target, enhances wound healing in a murine incisional wound model.

Tissue damage induces a reversible cell cycle arrest in G2, which promotes survival and mitogenic signals to facilitate tissue regeneration but drives senescence-like phenotypes under chronic stress conditions.

Myoglobin iron contributes to the formation and poor healing of muscle pressure injuries, that is, bedsores, and iron-chelation therapy can be administered after prolonged pressure to increase survival of the damaged tissue.

Isotonic treatment limits keratinocyte movement, spatially restricts reactive oxygen species production, and rescues sensory neuron function after thermal injury.

Transcriptional analyses provide an atlas of how traumatic brain injury and aging shape meningeal cell composition and gene expression.