BackgroundPrevious cohort studies investigating the association between sarcopenia and the risk of hospitalization have been inconsistent. We performed a meta-analysis to determine if sarcopenia is a predictor of hospitalization.MethodsProspective cohort studies that evaluated the association between sarcopenia and hospitalization in older people were identified via a systematic search of four electronic databases (PubMed, EMBASE, Science Citation Index, and the Cochrane Library). A random-effect model was applied to combine the results according to the heterogeneity of the included studies.ResultsFive studies (2832 participants) were included in this meta-analysis. Pooled results demonstrated that older people with sarcopenia were at an increased risk of hospitalization (pooled hazards ratio [HR] = 1.57, 95% confidence interval [CI] = 1.26, 1.94, I2 = 4.5%, P = 0.000) compared to those without sarcopenia. Results of subgroup analyses showed that hospitalized patients with sarcopenia had a higher rate of hospitalization (HR = 2.01, 95% CI = 1.41, 2.88, p = 0.000) versus patients without sarcopenia. A similar result was also found in community-dwelling older people with sarcopenia versus those without sarcopenia (HR = 1.40, 95% CI = 1.05, 1.88, p = 0.023). In addition, the subgroup analysis for length of follow-up showed that studies with a follow-up period of 3 years or more (pooled HR = 1.52, 95% CI = 1.19, 1.94, P = 0.001) reported a significantly higher rate of hospitalization among individuals with sarcopenia compared to those without sarcopenia. However, this association was not found in the studies with a follow-up period of less than 3 years (pooled HR = 1.76, 95% CI = 0.90, 3.44, P = 0.099).ConclusionsSarcopenia is a significant predictor of hospitalization among older individuals, and the association may not be significantly affected by the characteristics of the population or the definition of sarcopenia.Electronic supplementary materialThe online version of this article (10.1186/s12877-018-0878-0) contains supplementary material, which is available to authorized users.

Aging impairs the functions of human mesenchymal stem cells (MSCs), thereby severely reducing their beneficial effects on myocardial infarction (MI). MicroRNAs (miRNAs) play crucial roles in regulating the senescence of MSCs; however, the underlying mechanisms remain unclear. Here, we investigated the significance of miR-155-5p in regulating MSC senescence and whether inhibition of miR-155-5p could rejuvenate aged MSCs (AMSCs) to enhance their therapeutic efficacy for MI. Young MSCs (YMSCs) and AMSCs were isolated from young and aged donors, respectively. The cellular senescence of MSCs was evaluated by senescence-associated β-galactosidase (SA-β-gal) staining. Compared with YMSCs, AMSCs exhibited increased cellular senescence as evidenced by increased SA-β-gal activity and decreased proliferative capacity and paracrine effects. The expression of miR-155-5p was much higher in both serum and MSCs from aged donors than young donors. Upregulation of miR-155-5p in YMSCs led to increased cellular senescence, whereas downregulation of miR-155-5p decreased AMSC senescence. Mechanistically, miR-155-5p inhibited mitochondrial fission and increased mitochondrial fusion in MSCs via the AMPK signaling pathway, thereby resulting in cellular senescence by repressing the expression of Cab39. These effects were partially reversed by treatment with AMPK activator or mitofusin2-specific siRNA (Mfn2-siRNA). By enhancing angiogenesis and promoting cell survival, transplantation of anti-miR-155-5p-AMSCs led to improved cardiac function in an aged mouse model of MI compared with transplantation

Formation of aortic aneurysms as a consequence of augmented transforming growth factor β (TGF-β) signaling and vascular smooth muscle cell (VSMC) dysfunction is a potentially lethal complication of Marfan syndrome (MFS). Here, we examined VSMC senescence in patients with MFS and explored the potential mechanisms that link VSMC senescence and TGF-β. Tissue was harvested from the ascending aorta of control donors and MFS patients, and VSMCs were isolated. Senescence-associated β-galactosidase (SA-β-gal) activity and expression of senescence-related proteins (p53, p21) were significantly higher in aneurysmal tissue from MFS patients than in healthy aortic tissue from control donors. Compared to control-VSMCs, MFS-VSMCs were larger with higher levels of both SA-β-gal activity and mitochondrial reactive oxygen species (ROS). In addition, TGF-β1 levels were much higher in MFS- than control-VSMCs. TGF-β1 induced VSMC senescence through excessive ROS generation. This effect was suppressed by Mito-tempo, a mitochondria-targeted antioxidant, or SC-514, a NF-κB inhibitor. This suggests TGF-β1 induces VSMC senescence through ROS-mediated activation of NF-κB signaling. It thus appears that a TGF-β1/ROS/NF-κB axis may mediate VSMC senescence and aneurysm formation in MFS patients. This finding could serve as the basis for a novel strategy for treating aortic aneurysm in MFS.