ABSTRACT
Introduction: People with type 2 diabetes (T2D) are highly susceptible to the development of cardiovascular diseases. Previous studies have suggested that the application of vitamin D may offer potential benefits in improving lipid profiles, but these effects remain controversial. Methods: This systematic review and meta-analysis focused on the effects of vitamin D supplementation on serum lipid profiles in people with T2D. Randomized controlled trials (RCTs) assessing the effects of vitamin D supplementation on lipid profiles and published before September 19th, 2023, were identified in PubMed, Embase, and Cochrane Library. This review protocol was registered in the PROSPERO (CRD42023461136). The random-effects model was employed to estimate unstandardized mean differences (MD) and 95% confidence intervals (CIs). The quality of studies was assessed by the Cochrane Risk of Bias tool 2. Results: Overall, 20 RCTs involving 1711 participants were included. Results indicated that vitamin D supplementation significantly improves serum high-density lipoprotein (HDL) (MD: 1.63 mg/dL, 95% CI: 0.19 to 3.08, P = 0.03), and triglyceride (TG) levels (MD: -8.56 mg/dL, 95% CI: -15.23 to -1.89, P = 0.01). However, vitamin D supplementation failed to improve low-density lipoprotein (LDL) levels and total cholesterol (TC) levels. Subgroup analyses and meta-regressions suggested that higher doses of vitamin D supplementation and shorter duration of intervention were more likely to have favorable effects on lipid profiles. Moreover, participants with lower baseline BMI and higher serum 25-hydroxy vitamin D levels exhibited greater improvements in lipid profiles following vitamin D supplementation. Conclusions: This meta-analysis highlighted the effects of vitamin D supplementation on improving serum HDL and TG levels while not exhibiting significant improvements in LDL and TC levels. Further long-term and high-quality studies are still needed to draw more precise conclusions. Systematic review registration: https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=461136.
ABSTRACT
Spinal cord injury (SCI) is a result of a devastating injury to the central nervous system. Currently, there is no effective treatment available for these patients. The possible use of mesenchymal stem cell (MSC)-based treatment for SCI has been the focus of extensive investigations and is increasingly moving from the bench to bedside. Both experimental observations and clinical studies have shown the safety and efficacy of MSCs in managing SCI. However, the exact mechanism by which MSCs contribute to the repair of the injured spinal cord remains to be elucidated. In this review, we aim to summarize current research findings about the role of MSCs in improving complex pathology after SCI. MSCs exert a multimodal repair mechanism targeting multiple events in the secondary injury cascade. Our recent results showing the perineurium-like differentiation of surviving MSCs in the injured spinal cord may further the understanding of the fate of transplanted MSCs. These findings provide fundamental support for the clinical use of MSCs in SCI patients. Under experimental conditions, combining novel physical, chemical, and biological approaches led to significant improvements in the therapeutic efficacy of MSCs. These findings hold promise for the future of cell-based clinical treatment of SCI.
ABSTRACT
Multiple myeloma (MM) is a plasma cell neoplasm which is characterized by widespread genetic heterogeneity. The MMs with t(4;14) translocation exhibit poor outcomes. However, the mechanism underlying has not been well dissected. Our study aimed to identify key microRNA involved in the oncogenesis of t(4;14) MM. We here performed an integrated analysis to screen important regulators in the pathogenesis of t(4;14) MM. We used real-time quantitative polymerase chain reaction and western blotting to evaluate the mRNA and protein expression of the indicated microRNA or protein. Cell proliferation assay, colony formation assay, and transwell assay were used to examine the cell growth and metastasis. More importantly, the tumor growth and metastasis were analyzed in nude mice injected with MM cells. The integrated analysis indicated that miR-532 functioned as a pivotal regulator in t(4;14) MM. miR-532 was upregulated in t(4;14) MMs and promotes cell growth and metastasis in vitro and in vivo. Notably, though combing bioinformatics analysis and functional assays, CAMK2N1 was revealed as a functional target of miR-532 in MM cells. CAMK2N1 plays an anti-proliferative and anti-migration role in MM cells, and miR-532 exerts its oncogenic role though inhibiting CAMK2N1 expression in MMs. miR-532 promotes cell proliferation and invasion in t(4;14) MMs by targeting CAMK2N1. Our study, thus, provides possible targets for t(4;14) MM therapy.
