预约演示

更新于：2025-01-23

CILP

更新于：2025-01-23

基本信息

别名

cartilage intermediate layer protein、Cartilage intermediate layer protein 1、Cartilage intermediate layer protein 1 C1

+ [5]

简介

Probably plays a role in cartilage scaffolding. May act by antagonizing TGF-beta1 (TGFB1) and IGF1 functions. Has the ability to suppress IGF1-induced proliferation and sulfated proteoglycan synthesis, and inhibits ligand-induced IGF1R autophosphorylation. May inhibit TGFB1-mediated induction of cartilage matrix genes via its interaction with TGFB1. Overexpression may lead to impair chondrocyte growth and matrix repair and indirectly promote inorganic pyrophosphate (PPi) supersaturation in aging and osteoarthritis cartilage.

关联

项与 CILP 相关的药物

WO2024056833

专利挖掘

靶点

CILP

作用机制-

在研机构

Nordic Bioscience A/S

原研机构

Nordic Bioscience A/S

在研适应症

皮肤和肌肉骨骼疾病

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 CILP 相关的临床结果

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100 项与 CILP 相关的转化医学

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0 项与 CILP 相关的专利（医药）

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104

项与 CILP 相关的文献（医药）

2024-12-01·Journal of Cellular and Molecular Medicine

Regulation of Clusterin in the Heart and Plasma of Mice After Transverse Aortic Constriction

Article

作者: Chwastyniak, Maggy ; Weber, Lukas ; Turkieh, Annie ; Ernst, Matthias ; Pinet, Florence ; Beseme, Olivia ; Kiss, Attila ; Ye, Quianling ; Podesser, Bruno K. ; Amouyel, Philippe ; Baydar, Simge

ABSTRACTChronic pressure overload induces adverse cardiac remodelling characterised by left ventricular (LV) hypertrophy and fibrosis, leading to heart failure (HF). Identification of new biomarkers for adverse cardiac remodelling enables us to better understand this process and, consequently, to prevent HF. We recently identified clusterin (CLU) as a biomarker of cardiac remodelling and HF after myocardial infarction. The aim of this study was to investigate whether CLU expression is regulated in the heart and could be used as an indicator of adverse cardiac remodelling in response to pressure overload. We quantified CLU in the LV of mice subjected to transverse aortic constriction (TAC) and observed increased CLU mRNA levels and its mature protein form (m‐CLU) compared to the sham. Interestingly, CLU mRNA levels were positively correlated with pro‐hypertrophic (ANP, BNP, B‐MHC), pro‐ and anti‐fibrotic (TGFb, ColI and CILP) genes. In addition, m‐CLU was positively correlated with LV hypertrophy, LV end diastolic and systolic diameters, and negatively correlated with LV ejection fraction. Finally, we observed that m‐CLU levels only increased in TAC mice with severe cardiac remodelling and dysfunction without any significant difference in plasma CLU levels. This is the first study to demonstrate that cardiac expression of CLU is induced in the LV of TAC mice during adverse cardiac remodelling. However, plasma CLU levels could not be used as biomarkers of TAC‐induced cardiac remodelling and dysfunction.

2024-12-01·Molecular Biology Reports

Cholesterol associated genetic risk score and acute coronary syndrome in Czech males

Article

作者: Kettner, Jiri ; Adamkova, Vera ; Mrázková, Jolana ; Lanska, Vera ; Pitha, Jan ; Kautzner, Josef ; Staněk, Vladimir ; Gebauerová, Marie ; Hubacek, Jaroslav A

AbstractBackgroundDespite a general decline in mean levels across populations, LDL-cholesterol levels remain a major risk factor for acute coronary syndrome (ACS). The APOB, LDL-R, CILP, and SORT-1 genes have been shown to contain variants that have significant effects on plasma cholesterol levels.Methods and resultsWe examined polymorphisms within these genes in 1191 controls and 929 patients with ACS. Only rs646776 within SORT-1 was significantly associated with a risk of ACS (P < 0.05, AA vs. + G comparison; OR 1.21; 95% CI 1.01–1.45). With regard to genetic risk score (GRS), the presence of at least 7 alleles associated with elevated cholesterol levels was connected with increased risk (P < 0.01) of ACS (OR 1.26; 95% CI 1.06–1.52). Neither total mortality nor CVD mortality in ACS subjects (follow up—9.84 ± 3.82 years) was associated with the SNPs analysed or cholesterol-associated GRS.ConclusionsWe conclude that, based on only a few potent SNPs known to affect plasma cholesterol, GRS has the potential to predict ACS risk, but not ACS associated mortality.

2024-10-04·Journal of Proteome Research

Proteomics Analysis of Renal Cell Line Caki-2 with AFMID Overexpression and Potential Biomarker Discovery in Urine

Article

作者: Sun, Wei ; Xu, Jiyu ; Sun, Jiameng ; Guo, Zhengguang ; Chang, Jinchun ; Sun, Haidan ; Liu, Xiaoyan

Aromatic caninurine formamase (AFMID) is an enzyme involved in the tryptophan pathway, metabolizing N-formylkynurenine to kynurenine. AFMID had been found significantly downregulated in clear cell renal cell carcinoma (ccRCC) in both tissue and urine samples. Although ccRCC is characterized by a typical Warburg-like phenotype, mitochondrial dysfunction, and elevated fat deposition, it is unknown whether AFMID plays a role in tumorigenesis and the development of ccRCC. In the present study, AFMID overexpression had inhibitory effects for ccRCC cells, decreasing the rate of cell proliferation. Quantitative proteomics showed that AFMID overexpression altered cellular signaling pathways involved in cell growth and cellular metabolism pathways, including lipid metabolism and inositol phosphate metabolism. Further urine proteomic analysis indicated that cellular function dysfunction with AFMID overexpression could be reflected in the urine. The activity of predicted upregulators DDX58, TREX1, TGFB1, SMARCA4, and TNF in ccRCC cells and urine showed opposing change trends. Potential urinary biomarkers were tentatively discovered and further validated using an independent cohort. The protein panel of APOC3, UMOD, and CILP achieved an AUC value of 0.862 for the training cohort and 0.883 for the validation cohort. The present study is of significance in terms of highlighting various aspects of pathway changes associated with AFMID enzymes, discovering potential specific biomarkers for potential patient diagnosis, and therapeutic targeting.

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