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Updated: Oct 23, 2025
09:34
Study of Endoplasmic Reticulum and Mitochondria Interactions by In Situ Proximity Ligation Assay in Fixed Cells
Published on: December 10, 2016
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Abnormal Mitochondria-Endoplasmic Reticulum Communication Promotes Myocardial Infarction
Degang Cheng1, Jia Zheng1, Fang Hu1
1Department of Cardiology, Tianjin First Central Hospital, Tianjin, China.
Frontiers in Physiology
|August 20, 2021
Summary
Hypoxia triggers cardiomyocyte death via mitochondrial damage and endoplasmic reticulum stress, activating the JNK pathway. Inhibiting mitochondrial division protects against this damage, offering a potential therapeutic target for myocardial infarction.
Area of Science:
- Cardiovascular Biology
- Cellular Stress Response
- Mitochondrial Dynamics
Background:
- Myocardial infarction leads to cardiomyocyte death, worsened by mitochondrial and endoplasmic reticulum injury.
- The interplay between mitochondria and endoplasmic reticulum in cardiomyocyte death after infarction is not fully understood.
Purpose of the Study:
- To investigate the role of mitochondria-endoplasmic reticulum communication in cardiomyocyte death following myocardial infarction.
- To elucidate the molecular mechanisms linking hypoxia, mitochondrial dysfunction, and cell death.
Main Methods:
- Hypoxia treatment to mimic myocardial infarction conditions in cardiomyocytes.
- Investigated the role of the c-Jun N-terminal kinase (JNK) pathway.
- Assessed mitochondrial reactive oxygen species (mtROS) production and mitochondrial division.
- Utilized gene silencing of B cell receptor associated protein 31 (BAP31) and mitochondrial fission 1 (Fis1).
Main Results:
- Hypoxia induced cardiomyocyte death via JNK pathway activation.
- JNK activation was dependent on mtROS overproduction, triggered by mitochondrial division.
- Silencing BAP31 and Fis1 inhibited mitochondrial division, reduced mtROS, and prevented hypoxia-induced cardiomyocyte death.
- Identified a novel BAP31/Fis1/mtROS/JNK signaling axis in hypoxia-induced cell death.
Conclusions:
- Abnormal communication between mitochondria and endoplasmic reticulum, mediated by the BAP31/Fis1 axis, promotes cardiomyocyte death under hypoxic conditions.
- Targeting mitochondria-endoplasmic reticulum crosstalk presents a potential therapeutic strategy for myocardial infarction.
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