Muscle Physiology and Disorders

This study shows that DYSF in macrophages promotes STAT1 activation via calcium influx, impairing myogenesis and contributing to muscle atrophy with age.

This study uses machine learning to predict FSHD using multi-omics data and identifies key biomarkers, showing improved accuracy with limited samples.

This study identifies the Integrated Stress Response (ISR) pathway as a regulator of aged muscle stem cell activation and regeneration, showing pharmacological ISR activation improves their function and muscle repair.

This study identifies defective membrane repair and dysregulated annexin-A1/A2 expression in Duchenne muscular dystrophy, linking extracellular ANXA2 accumulation to disease severity.

This study shows mechanical loading induces muscle fiber growth through two mechanisms: mTORC1-dependent radial growth and mTORC1-independent longitudinal sarcomere addition.

This paper introduces FibeRtypeR, a tool to estimate muscle fiber type proportions from bulk transcriptomics and proteomics data using single-fiber reference profiles.

This study shows that ANTXR2 regulates COL6 turnover in skeletal muscle, and its deficiency leads to ECM stiffening and muscle dysfunction.

This study shows endothelial Piezo1 promotes mechanical overload-induced muscle hypertrophy by regulating AKT abundance, but not muscle regeneration.

This study identifies population-specific transcriptional changes in skeletal muscle myonuclei during pancreatic cancer cachexia, revealing distinct gene activation patterns rather than uniform upregulation of cachexia mediators.

The paper identifies a new subpopulation of aged muscle stem cells (GERI-MuSCs) that are senolytic-sensitive and rejuvenation-responsive, characterized by CD200 and CD63 markers.

This study examines how power-training and aging affect endomysium content and fiber cross-sectional area in human soleus muscle, finding no significant changes in endomysium but increased fiber area with training and aging.

This study uses chemogenetics to induce mitochondrial H2O2 in skeletal muscle and shows it causes dose-dependent atrophy without structural damage.

This study investigates cachexia-induced cardiac wasting using human iPSC-derived cardiac muscle, identifying the Atrogin-1/Calcineurin A/NFAT signaling pathway as a key driver of cardiac atrophy and functional impairments.

The paper identifies kranocytes as sensory platforms in neuromuscular junctions that connect adjacent junctions, interact with microvasculature, and respond to injury or disease.

This study shows CEBPβ regulates human myoblast proliferation and differentiation, and its altered expression contributes to defective myogenesis in FSHD.

This paper identifies Fibrillin-1 as a Notch-regulated matrix protein that maintains muscle stem cell quiescence by shielding them from mitogenic signals, and shows its loss leads to muscle dysfunction in Marfan syndrome.

This study shows that NRMT1 loss in C2C12 myoblasts disrupts muscle differentiation by altering gene expression related to cell cycle, muscle specification, and other lineage pathways.

This paper introduces a novel DMD mouse model with non-uniform dystrophin expression and shows that partial dystrophin expression protects against muscle pathology.

This study investigates JAG2-related muscular dystrophy by examining the role of Notch signaling in muscle stem cells, finding that JAG2 variants disrupt both autocrine and paracrine Notch signaling, impairing muscle regeneration.

The paper identifies a spatial gradient of Wnt signaling that restricts Mef2 expression in Drosophila muscle progenitors, maintaining a less committed state and preserving the progenitor pool.

This study shows that TRB3 overexpression in skeletal muscle reduces exercise-induced adaptations by impairing glucose metabolism and mitochondrial biogenesis.

The paper uses hiPSCs to study DMD, finding preserved cardiac dystrophin but reduced skeletal muscle dystrophin and cardiac Dp116 expression.

This study identifies transcriptomic changes in CKD muscle, showing suppressed immune and regenerative pathways, with 76 differentially expressed genes.

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

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.

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