|CSC-DC001925||Panoply™ Human C1QTNF3 Knockdown Stable Cell Line||Inquiry|
|CSC-SC001925||Panoply™ Human C1QTNF3 Over-expressing Stable Cell Line||Inquiry|
|CDCB170162||Danio rerio C1QTNF3 ORF Clone (NM_001020626)||Inquiry|
|CDCB194466||Rabbit C1QTNF3 ORF clone (XM_002714127.2)||Inquiry|
|CDCG012121||Mouse C1QTNF3 ORF clone(NM_030888.4)||Inquiry|
|CDCR038210||Mouse C1qtnf3 ORF clone (NM_001204134.1)||Inquiry|
|CDCR376846||Rat C1qtnf3 ORF Clone(NM_001134436.1)||Inquiry|
|CDCS416041||Human C1QTNF3 ORF Clone (BC016021)||Inquiry|
|CDCS416042||Human C1QTNF3 ORF Clone (BC120990)||Inquiry|
|CDCS416043||Human C1QTNF3 ORF Clone (BC112925)||Inquiry|
|CDFR009759||Rat C1qtnf3 cDNA Clone(NM_001134436.1)||Inquiry|
|MiUTR4H-TG00963||C1QTNF3 miRNA 3'UTR clone||Inquiry|
Recent Research Progress
The complement C1q tumor necrosis factor-related protein (CTRP) superfamily is a newly discovered adipokines cluster with a common structure consisting of collagen and globular C1q-like domains, and 15 human members have been identified. C1q / tumor necrosis factor-related protein-3 (CTRP3) belongs to the CTRP family, which is abundantly expressed in adipose tissue and chondrocytes. In 2011, CTRP3 was first reported to have comparable efficacy to adiponectin (APN) in vasodilation of C57BL mice. Circulating CTRP3 also improves insulin sensitivity and is closely related to glucose and lipid metabolism.
CTRP3 and DR
Diabetic retinopathy (DR) is a serious complication of chronic diabetes. CTRP has been shown to protect against obesity and atherosclerosis in animal studies. Studies have demonstrated that circulating CTRP3 can play a valuable role as a biomarker for diabetic retinopathy and can be an indicator of the severity of DR. Furthermore, CTRP3 inhibits high glucose high lipid (HGHL)-induced vascular cell adhesion molecule-1 (VCAM-1) expression in an AMP-activated protein kinase (AMPK)-dependent manner in human retinal microvascular endothelial cell (HRMEC), indicating a new therapeutic potential for CTRP3 in the treatment of DR, a serious and widespread complication of diabetes.
CTRP3 and obesity
Obesity has become a worldwide pandemic, with only two-thirds of adults in the United States being overweight or obese. Obesity alters the function of adipokines and leads to metabolic disorders. Obesity has been reported to cause atrophy of adipokines, including down-regulation of CTRP3. The results of Risa M et al. showed that adiponectin (APN) and CTRP3 levels were significantly lower in obese individual compared to lean controls; in addition, CTRP3 levels were positively correlated with adiponectin levels. In summary, studies have demonstrated a reduction in CTRP3 levels in human obesity. Obesity changes normal metabolic homeostasis and leads to dysregulation of adipokines production and function. CTRP3, or other adipokines, may be promising targets for the treatment of obesity and its associated comorbidities. Future investigations should include a larger study of multi-ethnic patients to further elucidate the interesting relationship between serum CTRP3 levels and ethnicity.
CTRP3 and CAD
CTRP3 may play a key role in the pathogenesis of coronary artery disease (CAD). Studies have shown that serum CTRP3 levels in CAD patients are significantly higher than non-CAD patients. Significant differences in CTRP3 levels were also found between the single vessel group and the trivascular group. Multiple logistic regression analysis showed that CTRP3 levels were associated with CAD with HDL cholesterol and glucose. These results indicate that CTRP3 may play an important role in the pathophysiology of CAD, suggesting that CTRP3 may represent a novel biomarker for CAD.
CTRP 3 and CD
Mesenteric adipose tissue hypertrophy, also known as "peristaltic fat" (inflamed adipose tissue enveloping the circumference of the gut), represents a sign of Crohn's disease (CD) and is present from the onset of the disease. Related connective tissue and adipose tissue changes are characterized by mesenteric fat hypertrophy, fibrosis, macrophage infiltration, local lymphadenopathy, tissue fibrosis, perivascular and transmural inflammation, and intimal/medial thickening of small vessels. The pathogenic and secondary effects of mesenteric adipose tissue inflammation in CD are controversial. Recently, studies have shown that CTRP3 is capable to modulate fibrotic processes of colon lamina propria fibroblasts (CLPF) from strictured intestinal tissues. By targeting TGF-b production and expression of the Expression of connective tissue growth factor (CTGF) and collagen I genes, CTRP3 reduces the fibrotic activity of fibrotic CD-CLPF. Based on this, CTRP3 can be considered as a novel molecular medium derived from intestinal/mesenteric adipose tissue, which inhibits CPLF activation and pro-fibrotic mechanisms. Thus, CTRP3 is an interesting and potential drug target for the pathophysiology of CD and its associated complications such as fibrosis and stenosis. Further research must clarify whether CTRP3 production in creep fat is altered compared to adipose tissue in non-IBD patients.
All in all, there is growing evidence that CTRPs have different biological effects on the cardiovascular system. In addition, CTRP3 has been reported to promote mitochondrial biogenesis in cardiomyocytes via the AMPK / peroxisome proliferators activated receptor-γ co-activator-1α (PGC1α) pathway. CTRP3 is an endogenous regulator of mitochondrial biogenesis that protects cardiomyocytes by improving mitochondrial dysfunction. Consequently, further research on CTRP3 is very valuable and meaningful.
Our promise to you:
Guaranteed product quality, expert customer support.
Contact us today for a free consultation with the scientific team and discover how Creative Biogene can be a valuable resource and partner for your organization.