Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Autophagic Cell Death01:18

Autophagic Cell Death

4.2K
Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
4.2K
Autophagy01:27

Autophagy

5.5K
Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
5.5K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

7.8K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
7.8K

You might also read

Related Articles

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

Sort by
Same author

Zinc-binding protein metallothionein 3 protects vascular smooth muscle cells from ferroptosis via blocking lysosomal degradation of GPX4.

Journal of molecular medicine (Berlin, Germany)·2026
Same author

HDAC8-selective inhibitor PCI-34051 protects against aortic dissection by attenuating ferroptosis of vascular smooth muscle cells.

Life medicine·2026
Same author

Altered weight-bearing compensatory neuromuscular control strategies in early-stage hip-related pain.

Frontiers in sports and active living·2026
Same author

Interactions between the gut microbiome and ferroptosis in degenerative diseases: Novel mechanisms and potential therapeutic strategies.

Acta pharmaceutica Sinica. B·2026
Same author

Elafibranor inhibits neointima formation by downregulating CDK1 expression in carotid artery injury mice model.

European journal of pharmacology·2026
Same author

ACAD8 deficiency promotes pathological cardiac hypertrophy in response to pressure overload by regulating histone isobutyrylation.

Nature communications·2026

Related Experiment Video

Updated: Dec 26, 2025

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
08:28

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Published on: February 15, 2022

4.2K

EHMT2/G9a Inhibits Aortic Smooth Muscle Cell Death by Suppressing Autophagy Activation.

Tai-Qiang Chen1, Nan Hu2, Bo Huo1

  • 1Division of Cardiothoracic and Vascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

International Journal of Biological Sciences
|March 17, 2020
PubMed
Summary

EHMT2 (G9a) regulates autophagic cell death in vascular smooth muscle cells. Inhibiting EHMT2 promotes cell death by increasing autophagosome formation, suggesting EHMT2 as a therapeutic target for cardiovascular diseases.

Keywords:
AutophagyBECN1EHMT2/G9aSQSTM1Vascular smooth muscle cells

More Related Videos

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
08:35

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells

Published on: June 12, 2017

10.6K
Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

9.0K

Related Experiment Videos

Last Updated: Dec 26, 2025

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
08:28

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Published on: February 15, 2022

4.2K
In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
08:35

In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells

Published on: June 12, 2017

10.6K
Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
09:18

Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death

Published on: December 27, 2016

9.0K

Area of Science:

  • Vascular Biology
  • Cell Death Mechanisms
  • Epigenetics

Background:

  • EHMT2 (G9a) is implicated in cancer and cardiac remodeling.
  • Its role in vascular smooth muscle cells (VSMCs) was previously unknown.

Purpose of the Study:

  • To investigate the function of EHMT2 in VSMCs.
  • To determine EHMT2's role in autophagic cell death (ACD).

Main Methods:

  • Inhibition of EHMT2 using BIX01294 or EHMT2 knockdown.
  • Assessment of VSMC proliferation, apoptosis, and autophagy markers (LC3II, autophagic vacuoles).
  • Analysis of SQSTM1 and BECN1 expression levels.

Main Results:

  • EHMT2 inhibition reduced VSMC numbers independently of proliferation and apoptosis.
  • EHMT2 levels decreased with autophagic inducers; inhibition increased autophagic vacuoles and LC3II.
  • EHMT2 suppressed ACD by inhibiting autophagosome formation, linked to SQSTM1 and BECN1 regulation.
  • Findings were validated in primary human aortic VSMCs.

Conclusions:

  • EHMT2 is a novel negative regulator of VSMC autophagic cell death.
  • EHMT2 inhibits ACD by suppressing autophagosome formation, partly via regulating SQSTM1 and BECN1.
  • EHMT2 inhibition presents a potential therapeutic strategy for cardiovascular diseases like aortic dissection.