In vitro, pretreatment of MRC5 human lung fibroblasts with GRg1 prior to exposure to cigarette smoke extract (CSE) reversed the cell ultrastructure disorder, decreased the expression of IL-6 and TNF-α, and significantly attenuated transdifferentiation of MRC5 cells by suppressing α-SMA and collagen I expression. Additionally, GRg1 suppressed the TGF-β1/Smad3 signaling pathway in CSE-stimulated MRC5 cells, whereas Smad3 over-expression abolished the anti-transdifferentiation effect of GRg1. In conclusion, the results of our study demonstrated that GRg1 improves lung function and protects against CS-induced airway remodeling, in part by down-regulating the TGF-β1/Smad3 signaling pathway. AJTR Copyright © 2020.Fatty acids (FAs) are potential therapeutic agents for cutaneous wound healing; however, the mechanisms underlying this effect have not been clearly defined. In this study, we extracted and characterized FAs from dried Lucilia sericata larvae and investigated the molecular basis by which FAs promote cutaneous wound healing. We first confirmed that FA sodium salts (FASSs) stimulated proliferation, migration, and tube formation of cultured human umbilical vein endothelial cells (HUVECs) in a dose-dependent manner. We then showed that FASSs promoted endothelial-to-mesenchymal transition (EndMT), which plays an important role in stabilizing the neovasculature during angiogenesis. Mechanistically, FASSs up-regulated the expression of angiogenesis-related growth factors, platelet-derived growth factor (PDGF), transforming growth factor-β1 (TGF-β1), and vascular endothelial growth factor A (VEGFA), and activated angiogenesis-related signaling pathways, AKT, ERK, and TGF-β/Smad3. In a rat acute cutaneous-wound model, FAs promoted wound healing. Following treatment, we further found that expression of anti-apoptosis-related factors (c-Myc and Bcl-2) was up-regulated and expression of apoptosis-related factors (p53 and Bad) was down-regulated. Our findings suggest that FAs can promote cutaneous wound healing by inducing angiogenesis, partly by activating AKT, ERK, and TGF-β/Smad3 signaling. AJTR Copyright © 2020.The dose-dependent pleiotropic effects of statin therapy may have unwanted side effects such as increasing the risk of intracerebral hemorrhage (ICH). The relationships among statin therapy, LDL-cholesterol levels, and ICH risk remain controversial. Here, we conduct a systematic review and meta-analysis of dose-dependent statin therapy and ICH risk. Eligible articles were identified by searching MEDLINE from inception up to December 1, 2018. Reference lists of previous meta-analyses were manually searched to retrieve all relevant publications. Statin doses were allocated into one of two groups according to the observed reduction of LDL cholesterol doses that lowered LDL-cholesterol levels ≥35% were regarded as high-dose statin therapy, whereas those that lowered LDL-cholesterol levels less then 35% were regarded as low-dose statin therapy. We retrieved 33 studies involving 203,305 subjects. The pooled analysis indicated that high-dose statin treatment significantly increased the risk of ICH [relative risk (RR), 1.35; 95% confidence interval (CI), 1.08-1.68] and reduced the risk of all stroke (RR, 0.85; 95% CI, 0.78-0.92), ischemic stroke (RR, 0.79; 95% CI, 0.72-0.87), and all-cause mortality (RR, 0.94; 95% CI, 0.90-0.98). The analyses did not detect any association between low-dose statin treatment and ICH (RR, 1.05; 95% CI, 0.88-1.25). Low-dose statin therapy significantly reduced the incidence of all stroke (RR, 0.84; 95% CI, 0.79-0.89), ischemic stroke (RR, 0.81; 95% CI, 0.76-0.86), and all-cause mortality (RR, 0.94; 95% CI, 0.92-0.97). Our data indicate that low-dose statin therapy is a safe and effective ICH treatment, whereas high-dose statin therapy is associated with increased ICH risk. Hence, our meta-analysis suggests that the dose-dependent pleiotropic effects of statin therapy are related to the measured reduction in LDL cholesterol. AJTR Copyright © 2020.PURPOSE SET binding protein 1 (SETBP1) has involved in cancer pathogenesis like leukemic malignancies and breast cancer. But the role and the underlying mechanism in NSCLC remain unclear. METHODS RT-PCR and western blotting were used for determining the expression level of SETBP1 in NSCLC. The clinical values of SETBP1 expression were evaluated by tissue microarray and immunohistochemistry. CCK-8, transwell and Matrigel assays were used to assess NSCLC cells proliferation, migration and invasion ability. The analysis of EMT markers was carried out by RT-PCR, western blotting and immunofluorescence. Bioinformatics analysis revealed the relationship between SETBP1 expression and tumor-associated immune cells. RESULTS SETBP1 expression was significantly downregulated in NSCLC tissues than matched peri-tumors and NSCLC patients with the decreased level of SETBP1 had worse OS. Downregulation of SETBP1 expression induced EMT to promote NSCLC cells proliferation, migration and invasion by the activation of ERK1/2 signal pathway. Aberrant SETBP1 expression was companied by disordered immune status of NSCLC patients and might be involved in regulation of polarization of tumor-associated macrophages. CONCLUSION SETBP1 can act as a tumor suppressor to reduce the progression of NSCLC and can be used for a prognostic biomarker in NSCLC. Aberrant SETBP1 expression was companied by disordered immune status of NSCLC patients. AJTR Copyright © 2020.Cancer cells reprogram their metabolism to adapt to fast growth and environmental demands, which differ them from normal cells. Mitochondria are central to the malignant metabolism reprogramming process. Here, we report that PPARα was highly expressed in gastric cancer tissues and negatively correlated with prognosis. Fenofibrate, a common drug used to treat severe hypertriglyceridemia and mixed dyslipidemia, reversed cellular metabolism and mitochondrial dysfunction in gastric cancer cells through PPARα.  https://www.selleckchem.com/products/Carboplatin.html  Our results show that fenofibrate altered glucose and lipid metabolism, inhibited gastric cancer cell proliferation, and promoted apoptosis in gastric cancer cells. We further show that fenofibrate induced mitochondrial reprogramming via CPT1 and the fatty acid oxidation pathway, as well as by activating the AMPK pathway and inhibiting the HK2 pathway. Additionally, fenofibrate inhibited subcutaneous gastric cancer cell tumor growth without obvious toxicity in mice. Collectively, our results indicate that fenofibrate exhibits anti-tumor activity in vitro and in vivo via the mitochondria and metabolic reprogramming, demonstrating that mitochondrial regulation and the normalization of cancer cell metabolism are novel therapeutic strategies for cancer.