Fig. 8: CTRP9–LAMP2A–NLRP3 axis is dysregulated in aged human primary myoblasts and restored by gCTRP9 treatment.
From: CTRP9 as a myokine mitigates sarcopenia via the LAMP-2A/NLRP3 pathway
A Representative immunofluorescence images of human primary myoblasts stained for MYOD1 (red), confirming their myogenic identity. Nuclei are counterstained with DAPI (blue). Scale bar = 50 μm. B SA-β-gal staining in primary myoblasts isolated from young and aged individuals (n = 3). Scale bar = 100 μm. C Western blot analysis of CTRP9, LAMP2A, and NLRP3 protein expression in young and aged human myoblasts; GAPDH serves as an internal reference (n = 3). D Quantification of SA-β-gal staining in siNC and siLAMP2A groups (n = 3). Scale bar = 100 μm. E Western blot analysis of NLRP3 expression following LAMP2A knockdown in human primary myoblasts; GAPDH serves as the loading control (n = 3). F SA-β-gal staining of aged human myoblasts treated with gCTRP9 (5 μg/mL, 24 h), (n = 3). Scale bar = 100 μm. G Western blot analysis of LAMP2A and NLRP3 expression in aged human myoblasts treated with gCTRP9; GAPDH serves as the loading control (n = 3). Data are presented as mean ± SEM.
