Zhi-ren Q. Zhang

State Key Laboratory Of Frigid Zone Cardiovascular Diseases
Harbin, China

Last Updated: 09/26/2026

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Found 58 publications

Inhibition of Programmed Cell Death-1 in Cytotoxic CD8+ T Cells Exacerbates Pressure Overload-Induced Cardiac Injury.

Inhibition of Programmed Cell Death-1 in Cytotoxic CD8+ T Cells Exacerbates Pressure Overload-Induced Cardiac Injury.

Journal: Circulation
Published: September 01, 2026

Research progress on the rapid reversal of atherosclerotic plaques by macrophage-targeted sonodynamic therapy

Research progress on the rapid reversal of atherosclerotic plaques by macrophage-targeted sonodynamic therapy

Journal: Zhonghua xin xue guan bing za zhi
Published: June 21, 2026

Corrigendum to "Smooth muscle cell (SMC) Specific SNRK deletion in mouse causes congenital short bowel syndrome and premature death" [Biochem. Biophys. Rep. 44 (2025) 102298].

Corrigendum to "Smooth muscle cell (SMC) Specific SNRK deletion in mouse causes congenital short bowel syndrome and premature death" [Biochem. Biophys. Rep. 44 (2025) 102298].

Journal: Biochemistry and biophysics reports
Published: March 23, 2026

Cardiovascular Safety of T Cell Engagers: Reassuring Overall, But Not Benign for All.

Cardiovascular Safety of T Cell Engagers: Reassuring Overall, But Not Benign for All.

Journal: JACC. CardioOncology
Published: March 12, 2026

Corrigendum to "MFN2-mediated decrease in mitochondria-associated endoplasmic reticulum membranes contributes to sunitinib-induced endothelial dysfunction and hypertension/JMCC 10006".

Corrigendum to "MFN2-mediated decrease in mitochondria-associated endoplasmic reticulum membranes contributes to sunitinib-induced endothelial dysfunction and hypertension/JMCC 10006".

Journal: Journal of molecular and cellular cardiology
Published: January 29, 2026

Smooth muscle cell (SMC)-Specific SNRK deletion in mouse causes congenital short bowel syndrome and premature death.

Smooth muscle cell (SMC)-Specific SNRK deletion in mouse causes congenital short bowel syndrome and premature death.

Journal: Biochemistry and biophysics reports
Published: July 11, 2025

Macrophage PD-1 regulates energy expenditure and metabolic dysfunction under immune checkpoint blockade.

Macrophage PD-1 regulates energy expenditure and metabolic dysfunction under immune checkpoint blockade.

Journal: Cell metabolism
Published: December 03, 2024

MFN2-mediated decrease in mitochondria-associated endoplasmic reticulum membranes contributes to sunitinib-induced endothelial dysfunction and hypertension.

MFN2-mediated decrease in mitochondria-associated endoplasmic reticulum membranes contributes to sunitinib-induced endothelial dysfunction and hypertension.

Journal: Journal of molecular and cellular cardiology
Published: July 30, 2024

Fusaric acid-mediated S-glutathionylation of MaAKT1 channel confers the virulence of Foc TR4 to banana.

Fusaric acid-mediated S-glutathionylation of MaAKT1 channel confers the virulence of Foc TR4 to banana.

Journal: PLoS pathogens
Published: July 19, 2024

KAT7 contributes to ponatinib-induced hypertension by promoting endothelial senescence and inflammatory responses through activating NF-κB signaling pathway.

KAT7 contributes to ponatinib-induced hypertension by promoting endothelial senescence and inflammatory responses through activating NF-κB signaling pathway.

Journal: Journal of hypertension
Published: July 14, 2024

Spexin Diminishes Atrial Fibrillation Vulnerability by Acting on Galanin Receptor 2.

Spexin Diminishes Atrial Fibrillation Vulnerability by Acting on Galanin Receptor 2.

Journal: Circulation
Published: May 10, 2024

Inhibition of CTLA-4 accelerates atherosclerosis in hyperlipidemic mice by modulating the Th1/Th2 balance via the NF-κB signaling pathway.

Inhibition of CTLA-4 accelerates atherosclerosis in hyperlipidemic mice by modulating the Th1/Th2 balance via the NF-κB signaling pathway.

Journal: Heliyon
Published: March 10, 2024
Showing 1-12 of 58

Last Updated: 09/26/2026