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We evaluated the number of CD26 expressing cells in peripheral blood of patients with COVID-19 within 72 h of admission and on day 4 and day 7 after enrollment. The majority of CD26 expressing cells were presented by CD3

Rapamycin (RAPA), an inhibitor of mTORC signaling, has been shown to extend life span in mice and other organisms. Recently, animal and human studies have suggested that inhibition of mTORC signaling can alleviate or prevent the development of cardiomyopathy. In view of this, we used a murine model of type 2 diabetes (T2D), BKS-Leprdb , to determine whether RAPA treatment can mitigate the development of T2D-induced cardiomyopathy in adult mice. Female BKS-Leprdb mice fed diet supplemented with RAPA from 11 to 27 weeks of age showed reduced weight gain and significant reductions of fat and lean mass compared with untreated mice. No differences in plasma glucose or insulin levels were observed between groups; however, RAPA-treated mice were more insulin sensitive (P < 0.01) than untreated mice. Urine albumin/creatinine ratio was lower in RAPA-treated mice, suggesting reduced diabetic nephropathy and improved kidney function. Echocardiography showed significantly reduced left ventricular wall thickness in mice treated with RAPA compared with untreated mice (P = 0.02) that was consistent with reduced heart weight/tibia length ratios, reduced myocyte size and cardiac fibrosis measured by histomorphology, and reduced mRNA expression of Col1a1, a marker for cardiomyopathy. Our results suggest that inhibition of mTORC signaling is a plausible strategy for ameliorating complications of obesity and T2D, including cardiomyopathy.

Adult cardiac stem cells can contribute to scar formation by acquiring myofibroblast phenotype in response to myocardial injury. Adenosine levels increase in ischemic hearts and modulate cardiac cell functions via binding to adenosine receptors (AR). Here, we tested the hypothesis that A2BAR regulate a reversible transition of cardiac Sca1+CD31- mesenchymal stem cells into a myofibroblast-like state in a mouse model of myocardial infarction (MI). Using flow cytometry, we found that MI resulted in a rapid increase in the numbers of alpha smooth muscle actin (αSMA)-positive Sca-1+CD31- cells by day 5, followed by gradual decline. Genetic ablation of A2BAR had no effect on accumulation of αSMA-positive Sca-1+CD31- cells. However, their numbers remained significantly higher in wild-type (WT) compared with A2BAR knockout (KO) hearts during their deactivation (by 1.2 and 2-fold on post-MI days 7 and 14, respectively; p