Muscle Physiology and Disorders

This study identifies exercise-induced anti-aging processes in skeletal muscle by analyzing intron retention and its link to genomic instability and mitochondrial function.

This study shows that reduced NR4A3 levels in skeletal muscle due to inactivity impair glucose metabolism, translation, and myotube size by affecting mTORC1 and ribosomal pathways.

This study identifies RCOR1 as a positive regulator of myogenesis and skeletal muscle regeneration by interacting with LSD1 and MyoD.

This study identifies early aging-related changes in muscle MERC ultrastructure and proteome, which are reversed by exercise, suggesting potential therapeutic targets for sarcopenia.

This study identifies transcriptional changes in black bears during hibernation that preserve muscle protein content through mTORC1 signaling and BCAA metabolism.

This study identifies a novel immune-vascular communication program in Drosophila that coordinates muscle maintenance after damage through macrophage-derived signals and ECM organization.

This study shows that TRIM32 loss in muscle cells delays differentiation by stabilizing c-Myc mRNA, contributing to LGMDR8 pathogenesis.

The paper identifies and characterizes quiescent stem cells in a non-human primate, showing their in vivo self-renewal and similarity to human cells.

This study examines age-related changes in serial sarcomere number across five hindlimb muscles in rats at four aging timepoints, finding significant SSN loss contributing to muscle mass decline.

The paper identifies Slit1 as a MET target gene that prevents premature differentiation during mammalian myogenesis by regulating progenitor cell migration and muscle development.

This paper develops a high-resolution kinematic method to quantify impaired mobility in dystrophic zebrafish larvae, finding significant differences in swimming performance between mutants and wild-types.

This study shows PSME3 regulates myoblast migration and differentiation by interacting with NUDC and modulating cell adhesion proteins, independent of proteasome activity.

This study shows that Parkin overexpression reduces muscle atrophy and improves mitochondrial bioenergetics but does not improve key histological features in a DMD mouse model.

This study identifies early impairments in satellite cells of a porcine DMD model using multi-omics analysis, showing intrinsic genetic defects rather than environmental factors.

The paper uses multi-omic profiling to study early regulatory changes in dexamethasone-induced muscle atrophy in C2C12 cells, identifying mitochondrial gene expression and alternative splicing alterations.

This study identifies endosomal pathway dysfunction in DMD muscle cells and shows that Rab5 upregulation contributes to endosomal defects, which can be mitigated by Rab5 knock-down or dystrophin restoration.

This study shows that fibrillin-related proteins regulate calcium homeostasis in dystrophic muscle across species, linking ECM integrity to calcium control.

This study uses proteomics to show sex-specific differences in mitochondrial protein response to exercise in a mouse model of FSHD, highlighting potential sex-specific biomarkers.

This study identifies TRIM72 as a novel MuRF1-interacting protein that contributes to impaired insulin signaling in skeletal muscle cells, linking MuRF1 to muscle atrophy and insulin resistance.

This study identifies fibro-adipogenic progenitors and macrophages as key players in elderly human skeletal muscle regeneration through spatial and single-cell transcriptomics, revealing their interplay via complement factor C3.

This study uses scRNA-seq to show that DMD satellite cells have molecular impairments and altered differentiation trajectories, leading to reduced regenerative capacity, with autophagy induction potentially rescuing differentiation.

The paper quantifies age-associated activity changes in DE50-MD dogs using accelerometers, finding reduced activity and increased rest time in affected dogs compared to controls.

This study uses a zebrafish model of Bethlem myopathy to show that collagen VI deficiency disrupts CaV1.1 function, leading to increased sarcoplasmic reticulum Ca2+ leak and muscle dysfunction.

This study identifies KLHL41's role in sarcomere assembly and muscle growth in zebrafish models of nemaline myopathy, revealing its importance in myofibril formation and cross-bridge regulation.

This study shows that inhibiting the TWEAK/Fn14 signaling reduces skeletal muscle wasting and tumor growth in cancer cachexia models.

The paper examines how chronic resistance training and acute fatigue affect passive viscoelastic properties of human skeletal muscle fibers, finding greater responsiveness in males than females.

This paper introduces a method called collablot to quantify collagen VI levels and structural disorganisation in cell cultures from patients with collagen VI-related dystrophies, showing its effectiveness in detecting treatment effects and structural changes.

This paper maps dystrophin isoform expression across human brain development and adulthood, revealing novel expression patterns in neurons and synapses.

The paper validates new genetic modifiers of Duchenne muscular dystrophy using a zebrafish CRISPR-based screening approach.

This study identifies CUL3-BTBD9 as an E3 ubiquitin ligase essential for myogenesis by ubiquitylating CAV1 and regulating insulin signaling in myoblasts.