Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Cardiac-derived CTRP9 protects against myocardial ischemia/reperfusion injury via calreticulin-dependent inhibition of apoptosis.

Cell death & disease - 20 Jun 2018

Zhao Dajun, Feng Pan, Sun Yang, Qin Zhigang, Zhang Zhengbin, Tan Yanzhen, Gao Erhe, Lau Wayne Bond, Ma Xinliang, Yang Jian, Yu Shiqiang, Xu Xuezeng, Yi Dinghua, Yi Wei

Abstract excerpt

Cardiokines play an essential role in maintaining normal cardiac functions and responding to acute myocardial injury. Studies have demonstrated the heart itself is a significant source of C1q/TNF-related protein 9 (CTRP9). However, the biological role of cardiac-derived CTRP9 remains unclear. We hypothesize cardiac-derived CTRP9 responds to acute myocardial ischemia/reperfusion (MI/R) injury as a cardiokine. We...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adiponectin
Share to Autocrine Communication

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Calreticulin

Share to Cardiotonic Agents

Share to Cyclic AMP-Dependent Protein Kinases

Share to Cyclic AMP Response Element-Binding Protein

Share to Heart Ventricles

Share to Myocardial Reperfusion Injury

Source

Open in PubMed Open full text

Identifiers

PMID: 29925877
DOI: 10.1038/s41419-018-0726-3
PMCID: PMC6010444

Genes

TNF

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Cardiac-derived CTRP9 protects against myocardial ischemia/reperfusion injury via calreticulin-dependent inhibition of apoptosis.PMID 29925877Read ↗

C1q/Tumor Necrosis Factor-Related Protein-9 Regulates the Fate of Implanted Mesenchymal Stem Cells and Mobilizes Their Protective Effects Against Ischemic Heart Injury via Multiple Novel Signaling Pathways.Semantic proximity Read ↗

Necroptosis: a significant and promising target for intervention of cardiovascular diseaseSemantic proximity Read ↗

Apoptosis in Cardiovascular Diseases: Mechanism and Clinical ImplicationsSemantic proximity Read ↗

CXADR-like membrane protein protects against heart injury by preventing excessive pyroptosis after myocardial infarction.Semantic proximity Read ↗

Protease-activated receptor-1 contributes to cardiac remodeling and hypertrophy.Semantic proximity Read ↗

The regulatory effect of Ca2+/calmodulin dependent protein kinase II mediated by receptor interacting protein kinase 3 on necroptosis of hypertrophic cardiomyocytesSemantic proximity Read ↗

Mas receptor activation regulates the functional phenotype of myocardial macrophages through the Akt/Nrf2 signaling pathway to alleviate sepsis-induced cardiomyopathy.Semantic proximity Read ↗

Potential targets for the treatment of MI: GRP75-mediated Ca<sup>2+</sup>transfer in MAMSemantic proximity Read ↗

A novel role for tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in the development of cardiac dysfunction and failure.Semantic proximity Read ↗

β-arrestin 2 mediates cardiac ischemia-reperfusion injury via inhibiting GPCR-independent cell survival signalling.Semantic proximity Read ↗

Caspase-9: A Multimodal Therapeutic Target With Diverse Cellular Expression in Human DiseaseSemantic proximity Read ↗

MicroRNA-532 protects the heart in acute myocardial infarction, and represses prss23, a positive regulator of endothelial-to-mesenchymal transition.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.