Murine periosteum is highly enriched for osteoprogenitors, many of which express αSMA, but fracture callus chondrocytes are partially derived from other sources.

Pericytes surrounding capillaries in the retina contain α-smooth muscle actin, demonstrating that pericytes have the necessary molecular machinery to change capillary diameter during neurovascular coupling.

Direct reprogramming of smooth muscle cells from HGPS patients revealed that BMP4 is a key contributor of vascular degeneration and might represent a new therapeutic target.

CRISPR/Cas9 gene editing in mice reveals that diverse functions of actin isoforms are defined by their nucleotide, rather than their amino acid sequence, suggesting a novel mechanism of nucleotide-dependent protein regulation in eukaryotic genomes.

Computational and theoretical biomechanical analysis reveals how actomyosin filaments and axial muscles conjugate their activity to realize a fourfold elongation during C. elegans embryogenesis, 4 hr just before hatching.

A new pathway is described involving the estrogen receptor alpha in the acute response of small arteries to flow independent of the ligand (estrogen) and of the nuclear signaling.

Gender-affirming hormone therapy in trans women leads to a loss of mature characteristics in the spermatogonial stem cell niche, causes spermatogenic arrest, and triggers fibrotic processes.

Gene knockout of liver fluke granulin by CRISPR/Cas9 attenuates the virulence of infection with a carcinogenic liver fluke.

Neutrophils use dorsal membrane protrusions of endothelial cells to cross the vascular wall.

Fat-body-specific loss of actin isoform Act5C disrupts fat body cell growth and fat storage, lipoprotein secretion, and insulin signaling, revealing a non-canonical role for the cortical actin cytoskeleton in nutrient signaling and inter-organelle trafficking.