Zhen-wei Pan

Harbin, China

Last Updated: 09/26/2026

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Found 34 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

Bclaf1 drives heart failure by recruiting Srsf2 to enhance Hand2 pre-mRNA splicing and pathological hypertrophy.

Bclaf1 drives heart failure by recruiting Srsf2 to enhance Hand2 pre-mRNA splicing and pathological hypertrophy.

Journal: Nature communications

Published: August 04, 2025

Cullin-associated and neddylation-dissociated protein 1 (CAND1) promotes cardiomyocyte proliferation and heart regeneration by enhancing the ubiquitinated degradation of Mps one binder kinase activator 1b (Mob1b).

Cullin-associated and neddylation-dissociated protein 1 (CAND1) promotes cardiomyocyte proliferation and heart regeneration by enhancing the ubiquitinated degradation of Mps one binder kinase activator 1b (Mob1b).

Journal: Cell death and differentiation

Published: December 12, 2024

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

eIF4A1 exacerbates myocardial ischemia-reperfusion injury in mice by promoting nuclear translocation of transgelin/p53.

eIF4A1 exacerbates myocardial ischemia-reperfusion injury in mice by promoting nuclear translocation of transgelin/p53.

Journal: Acta pharmacologica Sinica

Published: August 13, 2024

Anti-CTLA-4 m2a Antibody Exacerbates Cardiac Injury in Experimental Autoimmune Myocarditis Mice By Promoting Ccl5-Neutrophil Infiltration.

Anti-CTLA-4 m2a Antibody Exacerbates Cardiac Injury in Experimental Autoimmune Myocarditis Mice By Promoting Ccl5-Neutrophil Infiltration.

Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Published: January 13, 2024

Acetylcytidine modification of Amotl1 by N-acetyltransferase 10 contributes to cardiac fibrotic expansion in mice after myocardial infarction.

Acetylcytidine modification of Amotl1 by N-acetyltransferase 10 contributes to cardiac fibrotic expansion in mice after myocardial infarction.

Journal: Acta pharmacologica Sinica

Published: January 08, 2024

Deletion of ASPP1 in myofibroblasts alleviates myocardial fibrosis by reducing p53 degradation.

Deletion of ASPP1 in myofibroblasts alleviates myocardial fibrosis by reducing p53 degradation.

Journal: Nature communications

Published: December 05, 2023

Cullin-associated and neddylation-dissociated protein 1 (CAND1) alleviates NAFLD by reducing ubiquitinated degradation of ACAA2.

Cullin-associated and neddylation-dissociated protein 1 (CAND1) alleviates NAFLD by reducing ubiquitinated degradation of ACAA2.

Journal: Nature communications

Published: January 07, 2023

Substrate-dependent interaction of SPOP and RACK1 aggravates cardiac fibrosis following myocardial infarction.

Substrate-dependent interaction of SPOP and RACK1 aggravates cardiac fibrosis following myocardial infarction.

Journal: Cell chemical biology

Published: November 24, 2022

GDF11 promotes wound healing in diabetic mice via stimulating HIF-1ɑ-VEGF/SDF-1ɑ-mediated endothelial progenitor cell mobilization and neovascularization.

GDF11 promotes wound healing in diabetic mice via stimulating HIF-1ɑ-VEGF/SDF-1ɑ-mediated endothelial progenitor cell mobilization and neovascularization.

Journal: Acta pharmacologica Sinica

Published: June 14, 2022

Forced activation of dystrophin transcription by CRISPR/dCas9 reduced arrhythmia susceptibility via restoring membrane Nav1.5 distribution.

Forced activation of dystrophin transcription by CRISPR/dCas9 reduced arrhythmia susceptibility via restoring membrane Nav1.5 distribution.

Journal: Gene therapy

Published: October 22, 2021

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Last Updated: 09/26/2026