Aims Sarcopenia has been found to be frequently associated with co-morbidity among patients with heart failure (HF). However, there remain insufficient data to accurately estimate the global prevalence of sarcopenia in HF. Therefore, the purpose of this research was to conduct a systematic review and meta-analysis to estimate the current overall prevalence of sarcopenia in patients with HF. Methods and results We searched relevant databases for studies published up to 13 July 2020, assessing sarcopenia in vpatients with HF. After careful screening, data of included articles were extracted with a predesigned Excel form. Then the pooled prevalence of sarcopenia in patients with HF was calculated using the random-effects model. The Q test was used to assess the heterogeneity, and I 2 statistic was calculated to quantify and evaluate the heterogeneity. Subgroup analyses were conducted to determine potential sources of heterogeneity. A total of 2852 articles were initially identified, and after removing duplicate publications and applying the selection criteria, we reviewed 79 full-text articles. Finally, 11 articles (n = 1742 patients with HF) were included in this systematic review and meta-analysis. The pooled prevalence of sarcopenia in patients with HF was 34% [95% confidence interval (CI): 22-47%, I 2 = 96.59%] and ranged from 10% to 69%. However, substantial heterogeneity between studies (I 2 = 96.59%, P < 0.001) was observed. There was no significant heterogeneity between subgroups by sex (P = 0.803) or the method used to define sarcopenia (P = 0.307). While the heterogeneity between subgroups by population setting was statistically significant (P < 0.001), the pooled prevalence of sarcopenia was 55% (95% CI: 43-66%) for hospitalized patients with HF and 26% (95% CI: 16-37%) for ambulatory patients. Conclusions Sarcopenia was a common condition in patients with HF, and the prevalence of hospitalized patients was higher than for ambulatory patients. Early detection of sarcopenia was therefore important in patients with HF, and it was important to implement interventions so that physical therapists or managerial dieticians can easily be introduced into clinical practice.

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The aim of the present study was to examine the effects of proteasome inhibitor (PI)-induced autophagy on PC12 cells overexpressing A53T mutant α-synuclein (α-syn) by detecting alterations in the levels of microtubule-associated protein 1A/1B light chain (LC3)+ autophagosomes and the lysotracker-positive autolysosomes using immunofluorescence, the expression of LC3-II using western blot analysis and the morphology of PC12 cells using transmission electron microscopy. It was found that the addition of MG132 (500 nmol/l) significantly increased the number of autophagosomes and autolysosomes and upregulated the expression of LC3-II. The autophagy inhibitor 3-methyladenine (3-MA) completely inhibited the autophagy induced by MG132 (500 nmol/l). The autophagy enhancer trehalose significantly increased the number of autophagosomes and autolysosomes and improved the protein level of LC3-II induced by MG132. To examine the effect of PI-induced autophagy on the degradation of A53T mutant α-syn, the expression of α-syn was detected by western blot analysis. It was revealed that MG132 increased the expression of A53T α-syn and trehalose counteracted the increase of A53T α-syn induced by MG132. Combined inhibition of 3-MA and PI significantly increased the accumulation of A53T α-syn as compared with treatment using either single agent. In addition, combination of MG132 (500 nmol/l) with trehalose (50 mmol/l) or 3-MA (2 mmol/l) markedly decreased the cell viability as compared with treatment using either single agent individually as demonstrated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. These results suggest that the PI, MG132, could induce autophagy in PC12 cells overexpressing A53T mutant α-syn and this autophagy could be completely inhibited by 3-MA, indicating that PI-induced autophagy is mediated by the upregulation of the macroautophagy class III PI3K pathway. PI-induced autophagy may act as a compensatory degradation system for degradation of A53T α-syn when the ubiquitin-proteasome system is impaired. Autophagy activation may directly contribute to the survival of PC12 cells treated with proteasome inhibitors. The present study may assist in illuminating the association between PI and autophagy in the pathogenesis of Parkinson’s disease.

IFI16 is a tumour suppressor in HCC via activation of p53 signals and inflammasome.