Inflammation centered muscle signature of sarcopenia from postmenopausal women in Shanghai China.

Introduction: Sarcopenia reflects age-related failure of muscle maintenance and regeneration, with chronic low-grade inflammation disrupting the satellite cell niche. Validated tissue biomarkers that connect inflammaging to clinical phenotypes remain limited. We sought to define an inflammation-centered muscle transcriptomic signature in postmenopausal women from Shanghai China and to assess its association with case-control status and muscle phenotypes. Methods: We prospectively enrolled 20 women undergoing femoral fracture surgery including sarcopenia (n = 8) and controls (n = 12). Vastus lateralis biopsies underwent RNA sequencing. Differentially expressed genes were identified and intersected with inflammation-associated genes from GeneCards. Random-forest models prioritized a minimal marker set. Discrimination was assessed with receiver operating characteristic analysis. Associations with appendicular lean mass, handgrip strength and calf circumference were tested. Results: We detected 301 differentially expressed genes enriched for p53, MAPK, TNF and NF-κB signaling together with ubiquitin-mediated proteolysis and cellular senescence. Intersection with the inflammation catalogue yielded 22 candidates that separated cases from controls by unsupervised clustering. Random-forest ranking nominated a five-gene panel JUN, SOCS3, CP, PTEN and C4B that showed strong single-gene discrimination with areas under the curve from 0.830 to 0.906. Higher expression of these genes was inversely associated with muscle quantity and strength. Discussion: This work is a pilot study that delineates an inflammation-associated transcriptomic phenotype of sarcopenia in postmenopausal women. These markers nominate testable inflammatory pathways and provide a rationale for validation studies designed to determine whether non-invasive surrogates or larger cohorts can substantiate their translational relevance.