Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Necrosis

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

Regulation of the Unfolded Protein Response

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Dynamic Prediction of 3-Month Recurrence After First-Ever Ischemic Stroke Using a Two-Stream Attention-LSTM Model - Henan Province, China, 2025.

China CDC weekly·2026

Same author

Development and external validation of an interpretable machine learning model for early prediction of stroke-associated pneumonia: a multicenter study.

International journal of medical informatics·2026

Same author

Impact of PDCA cycle optimization on door-to-wire time in patients with acute st-segment elevation myocardial infarction: a single-center retrospective before-and-after QI study.

Heart & lung : the journal of critical care·2026

Same author

Development and validation of a machine learning model and a web tool for predicting the risk of Crohn's disease diagnosis in Chinese patients.

Public health·2026

Same author

Correction: Duodenal stricture in Crohn's disease successfully managed with a fully covered metal stent-assisted with double pig-tail stents.

Endoscopy·2026

Same author

Exploring the dynamics of symptom networks in esophageal cancer patients during chemotherapy: a cross-lagged panel network analysis.

European journal of oncology nursing : the official journal of European Oncology Nursing Society·2026

Search research articles

Related Experiment Video

Updated: Apr 28, 2026

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

MLKL Deficiency Stabilizes RIP3 and Aggravates Myocardial Injury by Promoting Apoptosis and Pyroptosis.

Ziguan Zhang¹, Zuheng Liu¹, Yilei Liu¹

¹Xiamen Key Laboratory of Cardiac Electrophysiology, Department of Cardiology, Xiamen Institute of Cardiovascular Diseases, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen 361003, China.

Current Issues in Molecular Biology

|April 27, 2026

Summary

Mixed lineage kinase domain-like protein (MLKL) deficiency unexpectedly worsened heart injury after myocardial infarction (MI). MLKL loss stabilizes RIP3, increasing cell death signaling and cardiac damage, suggesting RIP3 as a therapeutic target.

Keywords:

MLKL RIP3 apoptosis myocardial infarction pyroptosis

More Related Videos

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells

Published on: October 20, 2022

Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System

Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System

Published on: April 11, 2025

Related Experiment Videos

Last Updated: Apr 28, 2026

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells

Published on: October 20, 2022

Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System

Generation of a RIP1 Knockout U937 Cell Line Using the CRISPR-Cas9 System

Published on: April 11, 2025

Area of Science:

Cardiovascular Biology
Cell Death Pathways
Molecular Medicine

Background:

Regulated cardiomyocyte death significantly contributes to myocardial infarction (MI) injury.
The role of mixed lineage kinase domain-like protein (MLKL), a necroptosis effector, in MI is not fully understood.

Purpose of the Study:

To investigate the function of MLKL in myocardial infarction.
To elucidate the molecular mechanisms underlying MLKL's role in cardiac injury.

Main Methods:

MLKL expression analysis in hypoxic cardiomyocytes, infarcted murine hearts, and human cardiac tissue.
Functional studies using MLKL knockdown in cardiomyocytes and genetic deletion in mice subjected to MI.
Assessment of apoptosis and pyroptosis signaling pathways and RIP3 regulation.

Main Results:

MLKL expression increased in hypoxic cardiomyocytes, infarcted hearts, and failing human cardiac tissue.
MLKL deficiency aggravated myocardial injury, impaired cardiac function, and increased fibrosis post-MI.
MLKL deficiency led to RIP3 stabilization via impaired proteasomal degradation, enhancing apoptosis and pyroptosis signaling.

Conclusions:

MLKL deficiency promotes RIP3 stabilization and exacerbates cardiomyocyte death and myocardial injury following MI.
The MLKL-RIP3 axis plays a critical regulatory role in cardiomyocyte death.
Targeting RIP3 may offer a therapeutic strategy for myocardial infarction.