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

Activation of Aryl Hydrocarbon Receptor by ITE Improves Cardiac Function in Mice After Myocardial Infarction.

Journal of the American Heart Association - 6 Jul 2021

Seong Eunhwa, Lee Jun-Ho, Lim Sungmin, Park Eun-Hye, Kim Eunmin, Kim Chan Woo, Lee Eunmi, Oh Gyu-Chul, Choo Eun Ho, Hwang Byung-Hee, Kim Chan Joon, Ihm Sang Hyun, Youn Ho Joong, Chung Wook Sung, Chang Kiyuk

Abstract excerpt

Background The immune and inflammatory responses play a considerable role in left ventricular remodeling after myocardial infarction (MI). Binding of AhR (aryl hydrocarbon receptor) to its ligands modulates immune and inflammatory responses; however, the effects of AhR in the context of MI are unknown. Therefore, we evaluated the potential association between AhR and MI by treating mice with a nontoxic endogenous...

Read the complete abstract on PubMed

Topics

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

Share to Basic Helix-Loop-Helix Transcription Factors
Share to Coculture Techniques

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Receptors, Aryl Hydrocarbon

Share to Recovery of Function

Share to T-Lymphocytes, Regulatory

Share to Thiazoles

Share to Ventricular Function, Left

Share to Wound Healing

Source

Open in PubMed Open full text

Identifiers

PMID: 34157850
DOI: 10.1161/JAHA.120.020502
PMCID: PMC8403290

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

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

Activation of Aryl Hydrocarbon Receptor by ITE Improves Cardiac Function in Mice After Myocardial Infarction.PMID 34157850Read ↗

ROCK inhibitor Y-27632 down-regulates Il-1β expression in mice with experimental autoimmune myocarditisSemantic proximity Read ↗

Effects of Tranilast on Inflammasome and Macrophage Phenotype in a Mouse Model of Myocardial Infarction.Semantic proximity Read ↗

YAP/TAZ deficiency reprograms macrophage phenotype and improves infarct healing and cardiac function after myocardial infarction.Semantic proximity Read ↗

Tregs delivered post-myocardial infarction adopt an injury-specific phenotype promoting cardiac repair via macrophages in mice.Semantic proximity Read ↗

EPHB2 knockdown mitigated MI-induced myocardial injury by inhibiting MAPK signalingSemantic proximity Read ↗

Exogenous TGFβ1 and its mimic HpTGM attenuate the heart’s inflammatory response to ischaemic injury and improve long term cardiac outcomesSemantic proximity Read ↗

Cholinergic Stimulation Exerts Cardioprotective Effects and Alleviates Renal Inflammatory Responses after Acute Myocardial Infarction in Spontaneous Hypertensive Rats (SHRs)Semantic proximity Read ↗

Interleukin-38 alleviates cardiac remodelling after myocardial infarction.Semantic proximity Read ↗

Uremic toxin indoxyl sulfate induces trained immunity <i>via</i> the AhR-dependent arachidonic acid pathway in end-stage renal disease (ESRD)Semantic proximity Read ↗

Beneficial effects of selective HDL-raising gene transfer on survival, cardiac remodelling and cardiac function after myocardial infarction in miceSemantic proximity Read ↗

Protective role of 5-azacytidine on myocardial infarction is associated with modulation of macrophage phenotype and inhibition of fibrosis.Semantic proximity Read ↗

Conditional cardiac overexpression of endothelin-1 induces inflammation and dilated cardiomyopathy in mice.Semantic proximity Read ↗

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