Shi R. Jia

P.R. China
Beijing, 100191, China

Last Updated: 09/26/2026

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Found 22 publications

Mitophagy-mediated S1P facilitates muscle adaptive responses to endurance exercise through SPHK1-S1PR1/S1PR2 in slow-twitch myofibers.

Mitophagy-mediated S1P facilitates muscle adaptive responses to endurance exercise through SPHK1-S1PR1/S1PR2 in slow-twitch myofibers.

Journal: Autophagy

Published: April 04, 2025

Optoelectronic Oscillator-Based Microwave Photonic 20× Frequency Multiplier with Low Phase Noise.

Optoelectronic Oscillator-Based Microwave Photonic 20× Frequency Multiplier with Low Phase Noise.

Journal: Micromachines

Published: February 11, 2025

Mitochondria-derived vesicles serve as reactors in response to stress in cardiomyocytes.

Mitochondria-derived vesicles serve as reactors in response to stress in cardiomyocytes.

Journal: Cell communication and signaling : CCS

Published: January 08, 2025

TGF-β1/SMAD3 Regulates Programmed Cell Death 5 That Suppresses Cardiac Fibrosis Post-Myocardial Infarction by Inhibiting HDAC3.

TGF-β1/SMAD3 Regulates Programmed Cell Death 5 That Suppresses Cardiac Fibrosis Post-Myocardial Infarction by Inhibiting HDAC3.

Journal: Circulation research

Published: June 22, 2023

CMTM3 deficiency induces cardiac hypertrophy by regulating MAPK/ERK signaling.

CMTM3 deficiency induces cardiac hypertrophy by regulating MAPK/ERK signaling.

Journal: Biochemical and biophysical research communications

Published: March 28, 2023

FUNDC1-mediated mitophagy and HIF1α activation drives pulmonary hypertension during hypoxia.

FUNDC1-mediated mitophagy and HIF1α activation drives pulmonary hypertension during hypoxia.

Journal: Cell death & disease

Published: October 09, 2021

Mitophagy-regulated mitochondrial health strongly protects the heart against cardiac dysfunction after acute myocardial infarction.

Mitophagy-regulated mitochondrial health strongly protects the heart against cardiac dysfunction after acute myocardial infarction.

Journal: Journal of cellular and molecular medicine

Published: September 15, 2021

Programmed cell death 5 improves skeletal muscle insulin resistance by inhibiting IRS-1 ubiquitination through stabilization of MDM2.

Programmed cell death 5 improves skeletal muscle insulin resistance by inhibiting IRS-1 ubiquitination through stabilization of MDM2.

Journal: Life sciences

Published: April 19, 2021

The effectiveness of formative assessment in pathophysiology education from students' perspective: a questionnaire study.

The effectiveness of formative assessment in pathophysiology education from students' perspective: a questionnaire study.

Journal: Advances in physiology education

Published: November 06, 2020

Miro2 Regulates Inter-Mitochondrial Communication in the Heart and Protects Against TAC-Induced Cardiac Dysfunction.

Miro2 Regulates Inter-Mitochondrial Communication in the Heart and Protects Against TAC-Induced Cardiac Dysfunction.

Journal: Circulation research

Published: August 29, 2019

Programmed Cell Death 5 Provides Negative Feedback on Cardiac Hypertrophy Through the Stabilization of Sarco/Endoplasmic Reticulum Ca2+-ATPase 2a Protein.

Programmed Cell Death 5 Provides Negative Feedback on Cardiac Hypertrophy Through the Stabilization of Sarco/Endoplasmic Reticulum Ca2+-ATPase 2a Protein.

Journal: Hypertension (Dallas, Tex. : 1979)

Published: October 26, 2018

Nogo-C regulates post myocardial infarction fibrosis through the interaction with ER Ca2+ leakage channel Sec61α in mouse hearts.

Nogo-C regulates post myocardial infarction fibrosis through the interaction with ER Ca2+ leakage channel Sec61α in mouse hearts.

Journal: Cell death & disease

Published: January 26, 2018

Showing 1-12 of 22

Last Updated: 09/26/2026