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

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation

You might also read

Related Articles

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

Sort by

Same author

A chromosome-level genome assembly of the panda loach (Yaoshania pachychilus).

Scientific data·2026

Same author

Spatially Characterized Aortic Proteome Reveals Novel Regional Signatures and Glucocorticoid Receptor/Dipeptidase 1 Axis in Diabetic Vasculopathy.

MedComm·2026

Same author

Endothelial GPR68 Is Essential for Arteriogenesis and Represents a Therapeutic Target in a Model of Peripheral Artery Disease.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)·2026

Same author

Cognitive activation and emotional regulation effects of olfactory intervention in the context of advanced driver assistance systems.

Traffic injury prevention·2026

Same author

Endothelial TBK1 Deficiency Inhibits Endothelial-to-Mesenchymal Transition and Atherogenesis Through Suppressing PAK1/ERK1/2 Signaling.

Circulation research·2026

Same author

Endobronchial ultrasound-guided mediastinal biopsies for the diagnosis of mediastinal diseases: A network meta-analysis.

Pulmonology·2026

Search research articles

Related Experiment Video

Updated: May 26, 2025

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

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

Published on: February 15, 2022

ASH2L Deficiency in Smooth Muscle Drives Pulmonary Vascular Remodeling.

Jing Zhang¹, Xia Gu², Tian-Le Cheng¹

¹Department of Respiratory Disease, Xinqiao Hospital (J.Z., T.-L.C., Y.-J.Q., Y.F.), Third Military Medical University, Chongqing, China.

Circulation Research

|February 25, 2025

Summary

This summary is machine-generated.

ASH2L deficiency drives pulmonary hypertension (PH) by promoting smooth muscle cell proliferation and vascular remodeling. Targeting KLF5 offers a potential therapeutic strategy for PH.

Keywords:

RNA cell proliferation hypertension, pulmonary muscle, smooth vascular remodeling

More Related Videos

Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice

Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice

Published on: October 19, 2013

Utilizing the Precision-Cut Lung Slice to Study the Contractile Regulation of Airway and Intrapulmonary Arterial Smooth Muscle

Utilizing the Precision-Cut Lung Slice to Study the Contractile Regulation of Airway and Intrapulmonary Arterial Smooth Muscle

Published on: May 5, 2022

Related Experiment Videos

Last Updated: May 26, 2025

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

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

Published on: February 15, 2022

Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice

Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice

Published on: October 19, 2013

Utilizing the Precision-Cut Lung Slice to Study the Contractile Regulation of Airway and Intrapulmonary Arterial Smooth Muscle

Utilizing the Precision-Cut Lung Slice to Study the Contractile Regulation of Airway and Intrapulmonary Arterial Smooth Muscle

Published on: May 5, 2022

Area of Science:

Epigenetics
Molecular Biology
Cardiovascular Research

Background:

Histone H3 lysine 4 methylation is a key epigenetic mark implicated in vascular remodeling and pulmonary hypertension (PH).
SET1/MLL methyltransferase complexes are the primary enzymes for H3 lysine 4 methylation, but their specific roles in PH pathogenesis remain unclear.
ASH2L, a crucial component of SET1/MLL complexes, is investigated for its contribution to PH.

Purpose of the Study:

To investigate the role of ASH2L, a core SET1/MLL family member, in the pathogenesis of pulmonary hypertension (PH).
To elucidate the molecular mechanisms by which ASH2L influences vascular remodeling in PH.

Main Methods:

Analysis of human pulmonary artery specimens and primary vascular cells.
Utilized smooth muscle cell (SMC)-specific ASH2L-deficient mice and rats with ASH2L overexpression.
Employed mass spectrometry, immunoprecipitation, and chromatin immunoprecipitation assays.

Main Results:

ASH2L was the sole differentially expressed SET1/MLL family member in PH lung vessels, with decreased expression correlating with PH severity.
ASH2L depletion exacerbated SMC proliferation and vascular remodeling, while its restoration ameliorated these effects.
ASH2L regulated KLF5 degradation and NOTCH3 transcription independently of canonical H3 lysine 4 trimethylation, revealing a novel mechanism in PH.

Conclusions:

ASH2L deficiency promotes SMC proliferation and lung vascular remodeling in PH, partly via KLF5-dependent NOTCH3 transcription.
Therapeutic strategies targeting ASH2L activation or KLF5 inhibition show promise for treating PH.