Related Experiment Video

Updated: Apr 19, 2026

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

1.8K

TP53 links mitochondria-endoplasmic reticulum crosstalk and ferroptosis in septic cardiomyopathy: Protective

Jinshuai Lu1, Yuxia Tao2, Jinxian Li3

  • 1Department of Emergency, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi City 830001, Xinjiang, China.

Cellular Signalling
|April 17, 2026
PubMed
Abstract

Insights

Septic cardiomyopathy involves TP53-regulated ferroptosis and ER-mitochondria dysfunction. Nicorandil protects the heart by modulating TP53 signaling and ferroptosis, offering a potential therapeutic strategy.

Area of Science:

  • Cardiovascular Biology
  • Cellular Stress Response
  • Molecular Medicine

Background:

  • Septic cardiomyopathy (SCM) significantly contributes to sepsis mortality, lacking targeted therapies.
  • Ferroptosis and mitochondria-associated endoplasmic reticulum membranes (MAMs) are implicated in cardiac injury.
  • The role of TP53 in SCM, ferroptosis, and MAMs is not well understood.

Purpose of the Study:

  • Investigate TP53's role in MAM-associated ferroptosis in SCM.
  • Evaluate the cardioprotective effects of nicorandil (Nic) in SCM.

Main Methods:

  • Bioinformatics analysis identified key SCM genes.
  • Functional studies used LPS-induced H9C2 cells and a rat SCM model.
  • Assessed mitochondrial function, oxidative stress, calcium homeostasis, ferroptosis, and ER-mitochondria interactions with pharmacological and genetic interventions.

Main Results:

  • TP53 was identified as a hub gene linking ferroptosis and mitochondrial pathways in SCM.
  • LPS increased TP53, ER-mitochondria proximity, calcium dysregulation, oxidative stress, and ferroptosis.
  • Nic attenuated myocardial injury, reduced ferroptosis markers, and restored protective proteins; TP53 modulation affected these outcomes.

Conclusions:

  • TP53 is involved in SCM via MAM alterations, calcium dysregulation, and ferroptosis.
  • Nicorandil provides cardioprotection by modulating TP53-associated stress signaling and ferroptosis.
  • Targeting TP53-related stress pathways offers a potential therapeutic avenue for SCM.
Keywords:
Calcium homeostasisFerroptosisMitochondria–ER contactNicorandilSeptic cardiomyopathyTP53

More Related Videos

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation07:14

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation

Published on: July 13, 2018

15.5K
Analyzing Oxygen Consumption Rate in Primary Cultured Mouse Neonatal Cardiomyocytes Using an Extracellular Flux Analyzer11:26

Analyzing Oxygen Consumption Rate in Primary Cultured Mouse Neonatal Cardiomyocytes Using an Extracellular Flux Analyzer

Published on: February 13, 2019

9.3K

Related Concept Videos

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
19.8K
Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
628
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
13.8K
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
806
Cardiomyopathy IV: Restrictive Cardiomyopathy01:29

Cardiomyopathy IV: Restrictive Cardiomyopathy

Restrictive cardiomyopathy (RCM) is a rare heart muscle disease characterized by impaired ventricular filling due to stiffened ventricular walls, leading to significant diastolic dysfunction.EtiologyRestrictive cardiomyopathy can arise from both inherited and acquired diseases, many of which are systemic. It is categorized into four main types: infiltrative, storage, non-infiltrative, and endomyocardial diseases.Infiltrative diseases, such as amyloidosis, lead to RCM by depositing amyloid...
924