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Updated: Jun 25, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
Jumonji is a potential regulatory factor mediating nitric oxide-induced modulation of cardiac hypertrophy
Simon W Rabkin1, Shaun S Klassen
1Division of Cardiology, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada. rabkin@interchange.ubc.ca
Insights
Jumonji (jmj) protein may counteract cardiac hypertrophy by interacting with cell cycle regulators. Increasing jmj expression could be a therapeutic strategy for heart conditions.
Area of Science:
- Molecular Biology
- Cardiovascular Research
- Gene Regulation
Background:
- Jumonji (jmj) is a key protein in the jmj domain-containing family.
- It regulates genes involved in embryonic cardiac cell growth.
- Its role in the mature heart remains largely unknown.
Purpose of the Study:
- To investigate the function of jmj in the mature heart.
- To explore the role of jmj in cardiac hypertrophy.
- To understand the relationship between jmj, nitric oxide, and cardiac hypertrophy.
Main Methods:
- The study proposes interactions between JMJ domain 2A family proteins and cell cycle regulators (retinoblastoma protein, cyclin D, E2F).
- It examines the effect of nitric oxide on jmj gene and protein expression.
- The research focuses on the molecular mechanisms underlying cardiac hypertrophy modulation.
Main Results:
- The JMJ domain 2A family may modulate cardiac hypertrophy via interactions with cell cycle proteins, promoting cell growth.
- Nitric oxide can inhibit cardiac hypertrophy and upregulate jmj expression.
- jmj is identified as a potential mediator of nitric oxide's effects on cardiac hypertrophy.
Conclusions:
- jmj may act as a critical factor counteracting cardiac hypertrophy development.
- Biotechnology strategies to enhance jmj expression could offer a therapeutic approach.
- This research highlights a potential new target for mitigating cardiovascular disease associated with cardiac hypertrophy.
Background And Objectives:
Jumonji (jmj) is the prototypical member of the jmj domain-containing protein family. It regulates the expression of several genes, in particular genes involved in cardiac cell growth in the embryonic heart. The function of jmj in the mature or developed heart, however, is unclear.
Results:
We propose that JMJ domain 2A family may be involved in modulating the development of cardiac hypertrophy through interactions with cell cycle-regulatory proteins, specifically retinoblastoma protein, cyclin D and transcription factor E2F, that lead to cell growth. Because nitric oxide can block the development of cardiac hypertrophy and upregulate both jmj gene and protein expression, we propose that jmj is a novel regulatory factor mediating nitric oxide-induced modulation of cardiac hypertrophy.
Conclusion:
Jmj may be a critical, previously unrecognized factor that 'counteracts' the development of cardiac hypertrophy. Biotechnology approaches to increase its expression may be a potential therapeutic strategy to mitigate the increased cardiovascular morbidity and mortality associated with cardiac hypertrophy.
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