Repurposing of a drug designed for pain relief can quickly and reversibly slow biochemical and metabolic activities in cells and organs and could facilitate organ transplantation and prevent tissue injury.

Benchmark simulations show that the VEXAT muscle model is more accurate than a Hill-type muscle model at mimicking the response of biological muscle to length changes great and small.

Genetic mouse models combined with single-cell RNA sequencing reveal the essential role of SRSF2 in directing MyoD progenitors to distinct skeletal muscle domains and controlling their differentiation through the regulation of targeted genes and alternative splicing during skeletal muscle development.

Genetic reduction of Numb or Numb/Nubl is linked to deterioration of the Septin cytoskeleton and suggests cytoskeletal abnormalities are the consequences of and contribute to age-related changes in skeletal muscle.

Mutation E334Q in cytoskeletal γ-actin leads to impaired interaction of actin filaments with actin-binding proteins belonging to the myosin and ADF/cofilin families.

Intermittent fasting orchestrates molecular shifts, yielding cardiovascular improvements, revealing novel cardioprotective mechanisms, and suggesting innovative pharmacological strategies for cardiovascular disease prevention and treatment.

The balanced utilization of energy sources, namely carbohydrates and fats, by mitochondria, is critically important for the long-term maintenance of both skeletal muscle and heart health.

Caveolae and Bin1 form tubulation platforms.

Mice carrying a near-complete human chromosome 21 are hypermetabolic and have increased thermogenesis due to sarcolipin overexpression in the skeletal muscle, leading to persistent uncoupling of the sarco(endo)plasmic reticulum Ca²⁺ ATPase pump activity and heat generation.

Microtubule-dependent movement of the glucose transporter GLUT4 is important for insulin-stimulated muscle glucose uptake, involves the motor protein KIF5B, and is impaired in muscle from diet-induced obese mice.