Statin intake may be linked with a lower risk of several infectious diseases, including tuberculosis, which is an important cause of mortality worldwide. The aim of this study was to investigate the definite impacts of statins on the risk of tuberculosis (TB) in diabetic patients and in the general population. Methods: Four databases were thoroughly searched from inception up to July 2019. Articles in any language were included if they assessed and clarified statin intake, presented the risk of TB in diabetes mellitus (DM) patients or the general population, and reported odds ratios (ORs), relative risks (RRs), or hazard ratios (HRs) or contained data for relevant calculation. RRs with 95% confidence intervals (CIs) were pooled using random-effects models regardless of heterogeneity quantified by Cochran's Q and I 2 statistics. Results: Six articles reporting observational studies involving 2 073 968 patients were included. Four reported cohort studies, one a nested case-control study, and one was an abstract. Statin use significantly reduced the risk of TB in DM patients by 22% (pooled RR 0.78, 95% CI 0.63-0.95), with severe heterogeneity (I 2 = 76.1%). Statin intake also significantly decreased the risk of TB in the general population by 40% (pooled RR 0.60, 95% CI 0.50-0.71), with severe heterogeneity (I 2 = 57.7%). Conclusions: Statin use is related to a considerably lower risk of TB in both DM patients and the general population. However, these conclusions should be interpreted with caution given the possible remaining confounding, and call for large-size and multicenter randomized controlled studies in the future.

Abstract Acute aortic dissection (AAD) is a cardiovascular emergency caused by the formation of hematoma in the middle layer of the aortic wall. Adiponectin (APN) is an adipose tissue-specific protein that has anti-inflammation and anti-atherosclerosis functions. Pyroptosis, as an inflammatory cell death, depends on the activation of caspase1, while nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) is a typical representative of the pyroptosis pathway. In this study, we aimed to find whether APN affects the AAD process. The results showed that APN overexpression (OE) inhibited the AAD development and the levels of glucose, triglyceride, and total cholesterol in mice model. In addition, APN OE inhibited the productions of gasdermin D (GSDMD), NLRP3, caspase1, interleukin-1β (IL-1β), IL-18, and osteopontin (OPN), as well as α-smooth muscle actin (α-SMA) downregulation in vitro and in vivo. In addition, NLRP3 was found to be a target gene of miR-133a and miR-133a OE showed similar effects to APN OE in attenuating the LPS-induced productions of GSDMD, NLRP3, caspase1, IL-1β, IL-18, and OPN, as well as α-SMA downregulation in vascular smooth muscle cells (vSMCs). Moreover, the beneficial effects of APN OE were abolished by miR-133a knockdown in vSMCs. In conclusion, our present results indicated that the upregulation of miR-133a by APN inhibits pyroptosis pathway, which potentially rescues AAD.

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