Objective:To explore the relationship between serum C-reactive protein (CRP), transfor-ming growth factor-β 1 (TGF-β 1) levels and patients with primary Sj?gren's syndrome (pSS). Methods:Ninety patients with pSS (observation group) and 30 healthy people (control group) were recruited.The observation group was divided into 17 severe disease cases, 43 moderate disease cases and 30 mild cases.In the observation group, 54 cases were without lung interstitial change (ILD) and 36 cases were with ILD (including 15 in stageⅠ, 13 in stage Ⅱ and 8 in stage Ⅲ). The serum levels of CRP and TGF-β 1 were measured by enzyme-linked immuno sorbent assay (ELISA), and the relationship between the levels of CRP, TGF-β 1 and the severity of pSS and different stages of pulmonary interstitial disease was evaluated. Variance analysis, Student-Newman-Keuls (SNK)- q test or t test, Spearman rank correlation analysis were used for statistical analysis. Results:The serum CRP level of the observation group and the control group were [(13.5±7.8) mg/L] and [(3.5±1.1)] mg/L, respec-tively. The serum TGF-β 1 level of the observation group and the control group were [(61±14) μg/L] and [(28±9) μg/L], respectively ( t=6.980, P<0.01; t=12.086, P<0.01). In the observation group, the serum CRP concentrations of patients with moderate and severe disease were [(14.6±2.1) mg/L] and [(16.5±3.3) mg/L], the serum TGF-β 1 concentrations of patients with moderate and severe disease were[(61±13) μg/L] and [(76±18) μg/L], higher than those of patients with mild disease [(11.3±3.2) mg/L] and[(51±14) μg/L], and the level of patients with severe disease was increased more significantly ( F=3.634, P<0.01; F=4.661, P<0.01). The serum CRP and TGF-β 1 concentrations and disease severity were positively correlated ( r=0.786, P<0.01; r=0.516, P<0.01). The serum levels of CRP and TGF-β 1 in patients with pulmonary interstitial disease in the observation group [(15.5±3.2) mg/L and (74±19) μg/L] were higher than those without pulmonary interstitial disease [(10.5±2.2) mg/L and (51.6 ±13.8) μg/L] ( t=8.791, P<0.01; t=6.321, P<0.01). In the observation group, the serum CRP concentrations of patients with stage Ⅱ and stage Ⅲ of pulmonary interstitial disease were (16.3±8.2) mg/L and (19.1±10.1) mg/L, the serum TGF-β 1 concentrations of patients with stage Ⅱ and stage Ⅲ of pulmonary interstitial disease were [(74±19) μg/L and (85±21) μg/L], higher than those of patients with stage Ⅰ[(63±15) μg/L], and the serum CRP and TGF-β 1 concentrations of patients with stage Ⅲ were higher than those of patients with stage Ⅱ( F=4.640, P<0.01; F=5.673, P<0.01). There was a positive correlation between the serum CRP and TGF-β 1 concentrations of patients with pSS and the stages of pulmonary interstitial disease ( r=0.718, P<0.01, r=0.809, P<0.01). Conclusion:The serum levels of CRP and TGF-β 1 in patients with pSS are higher than those in healthy people. These two factors may be related to disease progress of pSS and the outcome of complicated pulmonary interstitial disease.

Several mitochondrial dysfunctions in obesity and diabetes include impaired mitochondrial membrane potential, excessive mitochondrial reactive oxygen species generation, reduced mitochondrial DNA, increased mitochondrial Ca2+ flux, and mitochondrial dynamics disorders. Mitophagy, specialized autophagy, is responsible for clearing dysfunctional mitochondria in physiological and pathological conditions. As a paradox, inhibition and activation of mitophagy have been observed in obesity and diabetes-related heart disorders, with both exerting bidirectional effects. Suppressed mitophagy is beneficial to mitochondrial homeostasis, also known as benign mitophagy. On the contrary, in most cases, excessive mitophagy is harmful to dysfunctional mitochondria elimination and thus is defined as detrimental mitophagy. In obesity and diabetes, two classical pathways appear to regulate mitophagy, including PTEN-induced putative kinase 1 (PINK1)/Parkin-dependent mitophagy and receptors/adapters-dependent mitophagy. After the pharmacologic interventions of mitophagy, mitochondrial morphology and function have been restored, and cell viability has been further improved. Herein, we summarize the mitochondrial dysfunction and mitophagy alterations in obesity and diabetes, as well as the underlying upstream mechanisms, in order to provide novel therapeutic strategies for the obesity and diabetes-related heart disorders.

Several mitochondrial dysfunctions in obesity and diabetes include impaired mitochondrial membrane potential, excessive mitochondrial reactive oxygen species generation, reduced mitochondrial DNA, increased mitochondrial Ca2+ flux, and mitochondrial dynamics disorders. Mitophagy, specialized autophagy, is responsible for clearing dysfunctional mitochondria in physiological and pathological conditions. As a paradox, inhibition and activation of mitophagy have been observed in obesity and diabetes-related heart disorders, with both exerting bidirectional effects. Suppressed mitophagy is beneficial to mitochondrial homeostasis, also known as benign mitophagy. On the contrary, in most cases, excessive mitophagy is harmful to dysfunctional mitochondria elimination and thus is defined as detrimental mitophagy. In obesity and diabetes, two classical pathways appear to regulate mitophagy, including PTEN-induced putative kinase 1 (PINK1)/Parkin-dependent mitophagy and receptors/adapters-dependent mitophagy. After the pharmacologic interventions of mitophagy, mitochondrial morphology and function have been restored, and cell viability has been further improved. Herein, we summarize the mitochondrial dysfunction and mitophagy alterations in obesity and diabetes, as well as the underlying upstream mechanisms, in order to provide novel therapeutic strategies for the obesity and diabetes-related heart disorders.

Several mitochondrial dysfunctions in obesity and diabetes include impaired mitochondrial membrane potential, excessive mitochondrial reactive oxygen species generation, reduced mitochondrial DNA, increased mitochondrial Ca2+ flux, and mitochondrial dynamics disorders. Mitophagy, specialized autophagy, is responsible for clearing dysfunctional mitochondria in physiological and pathological conditions. As a paradox, inhibition and activation of mitophagy have been observed in obesity and diabetes-related heart disorders, with both exerting bidirectional effects. Suppressed mitophagy is beneficial to mitochondrial homeostasis, also known as benign mitophagy. On the contrary, in most cases, excessive mitophagy is harmful to dysfunctional mitochondria elimination and thus is defined as detrimental mitophagy. In obesity and diabetes, two classical pathways appear to regulate mitophagy, including PTEN-induced putative kinase 1 (PINK1)/Parkin-dependent mitophagy and receptors/adapters-dependent mitophagy. After the pharmacologic interventions of mitophagy, mitochondrial morphology and function have been restored, and cell viability has been further improved. Herein, we summarize the mitochondrial dysfunction and mitophagy alterations in obesity and diabetes, as well as the underlying upstream mechanisms, in order to provide novel therapeutic strategies for the obesity and diabetes-related heart disorders.