Genetic mouse models identify a critical mechanism of myogenic vasoconstriction and reveal the in vivo function of myogenic autoregulation in protecting from organ overperfusion and in maintaining vascular resistance.

Extracellular matrix signaling constitutively regulates cerebral blood flow in both physiological and pathological settings.

Single myofiber ATAC-Seq provides assessment of chromatin accessibility of a single myofiber without the confounding effects of other cell types present in skeletal muscle.

Skeletal muscle organoids differentiated from human pluripotent stem cells offer a system for investigating myogenesis and satellite cell development with translational potential for muscular dystrophy modeling and therapy development.

Ablation of the Cdkn1c cell cycle inhibitor leads to defective muscle stem cell dynamics and myogenic potential, while progressive cytoplasmic to nuclear cellular localization of the Cdkn1c protein regulates growth arrest.

Promoter studies identified BMP/Smad signaling as a transcriptional regulator of Ppif gene encoding cyclophilin D, a component of the mitochondrial permeability transition pore, and gain- and loss-of-function experiments determined how such regulation affects osteogenic differentiation.

Cell encapsulation-based transcriptional profiling using myogenic progenitors reveals that long-range factors in the aged systemic environment induce a wide range of signaling pathways in a niche-independent manner.

Combined lineage-tracing strategies, single-cell transcriptomic methods and in situ analyses identified mesodermal bipotent progenitors during craniofacial myogenesis that give rise to myogenic and connective tissues, thus redefining the lineage and evolutionary relationships between muscle and associated stroma.

A computer model predicts different mechanisms of blood pressure regulation and effective hypertensive therapy for males and females, thereby serving as a foundational tool for improved treatment precision.

Genetic and biochemical analyses reveal that PERK is important for the survival of activated satellite stem cells during regeneration of injured skeletal muscle.