Yang Gong

238 Jiefang Road
Wuhan, 430060, China

Last Updated: 09/26/2026

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Found 13 publications

Phenylacetylglutamine exacerbates sepsis-induced cardiac dysfunction and left ventricular remodeling via the ferroptosis and TLR4/NF-κB pathway.

Phenylacetylglutamine exacerbates sepsis-induced cardiac dysfunction and left ventricular remodeling via the ferroptosis and TLR4/NF-κB pathway.

Journal: Frontiers in cardiovascular medicine

Published: May 01, 2026

The gut microbial metabolite phenylacetylglutamine exacerbates severe acute pancreatitis by promoting ferroptosis and TLR4/NF-κB signaling pathways.

The gut microbial metabolite phenylacetylglutamine exacerbates severe acute pancreatitis by promoting ferroptosis and TLR4/NF-κB signaling pathways.

Journal: International immunopharmacology

Published: December 15, 2025

The gut microbial metabolite phenylacetylglutamine increases susceptibility to atrial fibrillation after myocardial infarction through ferroptosis and NLRP3 inflammasome.

The gut microbial metabolite phenylacetylglutamine increases susceptibility to atrial fibrillation after myocardial infarction through ferroptosis and NLRP3 inflammasome.

Journal: Apoptosis : an international journal on programmed cell death

Published: November 15, 2024

4-octyl Itaconate Attenuates Acute Pancreatitis and Associated Lung Injury by Suppressing Ferroptosis in Mice.

4-octyl Itaconate Attenuates Acute Pancreatitis and Associated Lung Injury by Suppressing Ferroptosis in Mice.

Journal: Inflammation

Published: October 23, 2024

USP38 exacerbates myocardial injury and malignant ventricular arrhythmias after ischemia/reperfusion by promoting ferroptosis through the P53/SLC7A11 pathway.

USP38 exacerbates myocardial injury and malignant ventricular arrhythmias after ischemia/reperfusion by promoting ferroptosis through the P53/SLC7A11 pathway.

Journal: International immunopharmacology

Published: September 26, 2024

USP38 exacerbates atrial inflammation, fibrosis, and susceptibility to atrial fibrillation after myocardial infarction in mice.

USP38 exacerbates atrial inflammation, fibrosis, and susceptibility to atrial fibrillation after myocardial infarction in mice.

Journal: Molecular medicine (Cambridge, Mass.)

Published: July 03, 2023

USP38 regulates inflammatory cardiac remodeling after myocardial infarction.

USP38 regulates inflammatory cardiac remodeling after myocardial infarction.

Journal: Clinical science (London, England : 1979)

Published: July 03, 2023

Maresin1 ameliorates ventricular remodelling and arrhythmia in mice models of myocardial infarction via NRF2/HO-1 and TLR4/NF-kB signalling.

Maresin1 ameliorates ventricular remodelling and arrhythmia in mice models of myocardial infarction via NRF2/HO-1 and TLR4/NF-kB signalling.

Journal: International immunopharmacology

Published: August 24, 2022

Effect of sotagliflozin on ventricular arrhythmias in mice with myocardial infraction.

Effect of sotagliflozin on ventricular arrhythmias in mice with myocardial infraction.

Journal: European journal of pharmacology

Published: August 12, 2022

Dapagliflozin reduces pulmonary vascular damage and susceptibility to atrial fibrillation in right heart disease.

Dapagliflozin reduces pulmonary vascular damage and susceptibility to atrial fibrillation in right heart disease.

Journal: ESC heart failure

Published: March 25, 2022

Inhibition of ferroptosis reduces susceptibility to frequent excessive alcohol consumption-induced atrial fibrillation.

Inhibition of ferroptosis reduces susceptibility to frequent excessive alcohol consumption-induced atrial fibrillation.

Journal: Toxicology

Published: September 11, 2021

Ferroportin-mediated ferroptosis involved in new-onset atrial fibrillation with LPS-induced endotoxemia.

Ferroportin-mediated ferroptosis involved in new-onset atrial fibrillation with LPS-induced endotoxemia.

Journal: European journal of pharmacology

Published: June 02, 2021

Showing 1-12 of 13

Last Updated: 09/26/2026