Fig 2: Comparison of circulating irisin (A), FABP3 (B) and MIF (C) levels in healthy controls (N = 87) and patients with COPD (N = 86) and CHF (N = 81). The biomarkers levels were generally higher in the participants with advanced sarcopenia based on SPPB (D, E, and F) and SARC-F (G, H, and I) scoring. Values are expressed as mean ± SD, one-way analysis of variance. *p < 0.05.

Fig 3: Cumulative risk score for all the participants based on six biomarkers (P3NP, CAF22, osteonectin, irisin, FABP3 and MIF). The scatter plot of the participants with the median risk score (cutoff value = 3.86) was applied to divide into high- and low-risk groups (A). The relative proportion of the clinically diagnosed sarcopenic patients in the two risk-groups (B) and participants’ categorization based on SARC-F scores (C) in the three study cohorts. The relative proportion of the sarcopenic patients as defined by SARC-F criteria in the two risk-groups (D) in healthy controls and patients with COPD and CHF. *p < 0.05.

Fig 4: Alpelisib and fulvestrant induce cardiomyocyte injury, attenuated by dapagliflozin co-treatment. Human iPSC-derived cardiomyocytes were treated for 24 h with alpelisib (100 nM), fulvestrant (100 nM), or their combination, in the absence or presence of dapagliflozin (1 µM) under hyperglycemic conditions. (A) Heart-type fatty acid binding protein (H-FABP) and (B) cardiac troponin I levels were quantified in culture supernatants as markers of cardiomyocyte injury and normalized to total protein content where applicable. Drug treatments were associated with increased biomarker release, while dapagliflozin reduced these responses. Data are presented as mean ± SEM with individual data points representing independent biological replicates (n = 6). Statistical analysis was performed using two-way ANOVA followed by Tukey’s multiple-comparison test. * p < 0.05, *** p < 0.001, **** p < 0.0001; ns, not significant.