Lack of OPA1 in BAT impairs its thermogenic activation and induces endoplasmic reticulum stress, while improving systemic metabolism and thermoregulation via ATF4-FGF21-dependent and -independent mechanisms.
Single-cell analysis of injured mouse sciatic nerves reveals rapid reprogramming of macrophages toward a glycolytic, proinflammatory phenotype during the early repair process.
Malat1 is a key skeletal regulator, unveiling how lncRNAs integrate cellular crosstalk and molecular networks to regulate bone remodeling and regeneration, establishing a novel paradigm in tissue homeostasis and repair.