anti-C1q and Tumor Necrosis Factor Related Protein 9 (C1QTNF9) Antikörper

Human C1q and Tumor Necrosis Factor Related Protein 9 (C1QTNF9) Interaktionspartner

1. CTRP9 inhibits the cholesterol-induced Vascular smooth muscle cell phenotype switch and cell dysfunction by activating PRKAA1 (zeige PRKAA1 Antikörper).

2. results revealed increased circulating levels of CTRP9 in T2DM and CAD (zeige CAD Antikörper) individuals which suggests a compensatory response to insulin (zeige INS Antikörper) resistance, inflammatory milieu and endothelial dysfunction; however, more studies are needed to confirm this

3. CTRP9 levels are elevated in obesity and significantly decrease following weight loss surgery.

4. Plasma CTRP9 levels are associated with atherosclerosis in diabetic patients without CKD, independently of obesity, adiponectin, and traditional cardiovascular risk factors

5. The up-regulation of CTRP9 during hypertrophic heart disease facilitates maladaptive cardiac remodeling and left ventricular dysfunction.

6. Results demonstrate that CTRP9 alleviates hepatic steatosis through relief of endoplasmic reticulum stress via the AMPK (zeige PRKAA1 Antikörper)-mediated induction of autophagy.

7. Study demonstrates that CTRP9 attenuates cytokine-induced vascular inflammation in endothelial cells mediated by AMPK (zeige PRKAA1 Antikörper) activation.

8. Circulating and coronary CTRP9 plays an important role in the inflammation and coronary atherosclerosis of CAD (zeige CAD Antikörper) patients. Serum CTRP9 is an independent protective factor of CAD (zeige CAD Antikörper)

9. Serum CTRP9 concentration was significantly and positively associated with arterial stiffness in patients with type 2 diabetes

10. Serum CTRP9 concentrations were positively associated with favorable glucose or metabolic phenotypes and absence of metabolic syndrome, independent of serum total adiponectin concentrations.

Mouse (Murine) C1q and Tumor Necrosis Factor Related Protein 9 (C1QTNF9) Interaktionspartner

1. CTRP9 is a cardiokine critical in maintaining a healthy microenvironment facilitating stem cell engraftment in infarcted myocardial tissue treated with mesenchymal stem cell transplantation.

2. Based on these findings, this study showed that CTRP9 might induce mitochondrial biogenesis and protect high glucose-induced endothelial oxidative damage via AdipoR1-SIRT1-PGC-1alpha signaling pathway.

3. These results suggested that gCTRP9 protected RAW 264.7 macrophages from oxLDL via AMPK (zeige PRKAA1 Antikörper) activation in an AdipoR1 (zeige ADIPOR1 Antikörper) dependent fashion.

4. Suggest reduced plasma CTRP9 concentration during diabetes plays a causative role in platelet hyper-activity, contributing to platelet-induced cardiovascular damage.

5. Results demonstrate that CTRP9 alleviates hepatic steatosis through relief of endoplasmic reticulum stress via the AMPK (zeige PRKAA1 Antikörper)-mediated induction of autophagy.

6. Enhancing cardiac CTRP9 production and/or its proteolytic posttranslational modification are of therapeutic potential, attenuating diabetic cardiac injury.

7. CTRP9 protects against acute cardiac damage in response to pathological stimuli by suppressing inflammatory reactions through AdipoR1 (zeige ADIPOR1 Antikörper)/AMPK (zeige PRKAA1 Antikörper)-dependent mechanisms.

8. CTRP9 reduces pro-inflammatory cytokines expression in atherosclerotic plaque.

9. Genetic evidence for a physiological role of CTRP9 in controlling energy balance via central and peripheral mechanisms.

10. Adipokine CTRP9 attenuates adverse cardiac remodeling after acute myocardial infarction, largely via a protein kinase A (PKA)-dependent pathway.