SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Wu XK) "

Sökning: WFRF:(Wu XK)

  • Resultat 1-30 av 30
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  •  
2.
  •  
3.
  •  
4.
  •  
5.
  •  
6.
  •  
7.
  •  
8.
  • Sun, XT, et al. (författare)
  • Inflammatory cell-derived CXCL3 promotes pancreatic cancer metastasis through a novel myofibroblast-hijacked cancer escape mechanism
  • 2022
  • Ingår i: Gut. - : BMJ. - 1468-3288 .- 0017-5749. ; 71:1, s. 129-147
  • Tidskriftsartikel (refereegranskat)abstract
    • Pancreatic ductal adenocarcinoma (PDAC) is the most lethal malignancy and lacks effective treatment. We aimed to understand molecular mechanisms of the intertwined interactions between tumour stromal components in metastasis and to provide a new paradigm for PDAC therapy.DesignTwo unselected cohorts of 154 and 20 patients with PDAC were subjected to correlation between interleukin (IL)-33 and CXCL3 levels and survivals. Unbiased expression profiling, and genetic and pharmacological gain-of-function and loss-of-function approaches were employed to identify molecular signalling in tumour-associated macrophages (TAMs) and myofibroblastic cancer-associated fibroblasts (myoCAFs). The role of the IL-33–ST2–CXCL3–CXCR2 axis in PDAC metastasis was evaluated in three clinically relevant mouse PDAC models.ResultsIL-33 was specifically elevated in human PDACs and positively correlated with tumour inflammation in human patients with PDAC. CXCL3 was highly upregulated in IL-33-stimulated macrophages that were the primary source of CXCL3. CXCL3 was correlated with poor survival in human patients with PDAC. Mechanistically, activation of the IL-33–ST2–MYC pathway attributed to high CXCL3 production. The highest level of CXCL3 was found in PDAC relative to other cancer types and its receptor CXCR2 was almost exclusively expressed in CAFs. Activation of CXCR2 by CXCL3 induced a CAF-to-myoCAF transition and α-smooth muscle actin (α-SMA) was uniquely upregulated by the CXCL3–CXCR2 signalling. Type III collagen was identified as the CXCL3–CXCR2-targeted adhesive molecule responsible for myoCAF-driven PDAC metastasis.ConclusionsOur work provides novel mechanistic insights into understanding PDAC metastasis by the TAM-CAF interaction and targeting each of these signalling components would provide an attractive and new paradigm for treating pancreatic cancer.
  •  
9.
  •  
10.
  •  
11.
  •  
12.
  •  
13.
  •  
14.
  •  
15.
  •  
16.
  •  
17.
  • Du, QQ, et al. (författare)
  • Generation of mega brown adipose tissue in adults by controlling brown adipocyte differentiation in vivo
  • 2022
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490. ; 119:40, s. e2203307119-
  • Tidskriftsartikel (refereegranskat)abstract
    • Brown adipose tissue (BAT) is a highly specialized adipose tissue in its immobile location and size during the entire adulthood. In response to cold exposure and other β3-adrenoreceptor stimuli, BAT commits energy consumption by nonshivering thermogenesis (NST). However, the molecular machinery in controlling the BAT mass in adults is unknown. Here, we show our surprising findings that the BAT mass and functions can be manipulated in adult animals by controlling BAT adipocyte differentiation in vivo. Platelet-derived growth factor receptor α (PDGFα) expressed in BAT progenitor cells served a signaling function to avert adipose progenitor differentiation. Genetic and pharmacological loss-of-function of PDGFRα eliminated the differentiation barrier and permitted progenitor cell differentiation to mature and functional BAT adipocytes. Consequently, an enlarged BAT mass (megaBAT) was created by PDGFRα inhibition owing to increases of brown adipocyte numbers. Under cold exposure, a microRNA-485 (miR-485) was identified as a master suppressor of the PDGFRα signaling, and delivery of miR-485 also produced megaBAT in adult animals. Noticeably, megaBAT markedly improved global metabolism, insulin sensitivity, high-fat-diet (HFD)-induced obesity, and diabetes by enhancing NST. Together, our findings demonstrate that the adult BAT mass can be increased by blocking the previously unprecedented inhibitory signaling for BAT progenitor cell differentiation. Thus, blocking the PDGFRα for the generation of megaBAT provides an attractive strategy for treating obesity and type 2 diabetes mellitus (T2DM).
  •  
18.
  •  
19.
  •  
20.
  •  
21.
  • Hosaka, K, et al. (författare)
  • Therapeutic paradigm of dual targeting VEGF and PDGF for effectively treating FGF-2 off-target tumors
  • 2020
  • Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 11:1, s. 3704-
  • Tidskriftsartikel (refereegranskat)abstract
    • FGF-2 displays multifarious functions in regulation of angiogenesis and vascular remodeling. However, effective drugs for treating FGF-2+ tumors are unavailable. Here we show that FGF-2 modulates tumor vessels by recruiting NG2+ pricytes onto tumor microvessels through a PDGFRβ-dependent mechanism. FGF-2+ tumors are intrinsically resistant to clinically available drugs targeting VEGF and PDGF. Surprisingly, dual targeting the VEGF and PDGF signaling produces a superior antitumor effect in FGF-2+ breast cancer and fibrosarcoma models. Mechanistically, inhibition of PDGFRβ ablates FGF-2-recruited perivascular coverage, exposing anti-VEGF agents to inhibit vascular sprouting. These findings show that the off-target FGF-2 is a resistant biomarker for anti-VEGF and anti-PDGF monotherapy, but a highly beneficial marker for combination therapy. Our data shed light on mechanistic interactions between various angiogenic and remodeling factors in tumor neovascularization. Optimization of antiangiogenic drugs with different principles could produce therapeutic benefits for treating their resistant off-target cancers.
  •  
22.
  •  
23.
  •  
24.
  •  
25.
  •  
26.
  •  
27.
  •  
28.
  •  
29.
  • Zhe, XW, et al. (författare)
  • Hypertriglyceridemic waist is associated with increased carotid atherosclerosis in chronic kidney disease patients
  • 2012
  • Ingår i: Nephron. Clinical practice. - : S. Karger AG. - 1660-2110. ; 122:3-4, s. 146-152
  • Tidskriftsartikel (refereegranskat)abstract
    • <b><i>Background:</i></b> Patients with chronic kidney disease (CKD) have an unacceptably high risk of death, primarily as a result of cardiovascular disease (CVD). The ‘hypertriglyceridemic waist' phenotype has been proposed as a simple and strong predictor of CVD risk. Therefore, we investigated the relationship between the hypertriglyceridemic waist phenotype and carotid atherosclerosis in CKD patients. <b><i>Methods:</i></b> In a cross-sectional study, we enrolled 785 prevalent CKD patients [416 males, aged 44.6 years (21.7-69.4), glomerular filtration rate 52.5 ml/min/1.73 m<sup>2</sup> (5.3-119.4)]. We divided the patients into three groups: group 1: waist circumference >90 cm in men or >85 cm in women and triglycerides ≥2 mmol/l (n = 109); group 3: waist circumference ≤90 cm in men or ≤85 cm in women and triglycerides <2 mmol/l (n = 379), and group 2: the remaining patients (n = 297). Routine biochemical parameters and carotid artery intima-media thickness (IMT) were measured. <b><i>Results:</i></b> The prevalence of the hypertriglyceridemic waist phenotypes was 13.8% in the CKD patients. Triglyceride, total cholesterol, HDL-cholesterol and LDL-cholesterol concentrations in group 1 were significantly higher than those in group 3. Carotid artery IMT of the hypertriglyceridemic waist group was the highest. <b><i>Conclusion:</i></b> The hypertriglyceridemic waist phenotype was associated with worse carotid atherosclerosis in CKD patients. This suggests that the hypertriglyceridemic waist phenotype may be useful for predicting CVD risk in CKD patients.
  •  
30.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-30 av 30

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy