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January 1, 2023Theranostics76 citationsOpen Access

OTUD1 promotes pathological cardiac remodeling and heart failure by targeting STAT3 in cardiomyocytes

MWMengyang WangXHXue HanTYTianxiang Yu

Key Result

OTUD1 knockout significantly protected mice against angiotensin II- and transverse aortic constriction-induced cardiac dysfunction, hypertrophy, and fibrosis by modulating STAT3 activity.

Structured PICO

Does OTUD1 promote pathological cardiac remodeling and heart failure by targeting STAT3 in cardiomyocytes?

P
Population
Preclinical study using male wild-type and OTUD1 knockout mice to investigate the mechanisms of hypertensive cardiac remodeling and heart failure.
I
Intervention
OTUD1 knockout, OTUD1 overexpression via AAV9, or OTUD1 silencing via siRNA in the setting of Angiotensin II infusion or transverse aortic constriction (TAC).
C
Comparator
Wildtype mice, empty vector (AAV9-NC), or scrambled siRNA with saline infusion or sham operation.
O
Outcome
Cardiac hypertrophy, fibrosis, and dysfunction (measured by echocardiography, histological staining, and molecular markers).surrogate

OTUD1 promotes pathological cardiac remodeling and heart failure by deubiquitinating STAT3, suggesting OTUD1 as a potential therapeutic target for hypertensive heart failure.

Limitations

  • Preclinical animal and in vitro models may not fully translate to human clinical pathology.

Abstract

Cardiomyocyte OTUD1 promotes pathological cardiac remodeling and dysfunction by deubiquitinating STAT3. These studies have highlighted a novel role of OTUD1 in hypertensive heart failure and identified STAT3 as a target of OTUD1 in mediating these actions.

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Cite This Study

Wang et al. (2023) studied Heart failure and cardiac remodeling. OTUD1 knockout vs. Wild-type mice was evaluated on Cardiac dysfunction, hypertrophy, and fibrosis induced by Ang II or TAC. OTUD1 knockout significantly protected mice against angiotensin II- and transverse aortic constriction-induced cardiac dysfunction, hypertrophy, and fibrosis by modulating STAT3 activity.

synapsesocial.com/papers/6a4310d581106ce71fa75c58https://doi.org/10.7150/thno.83340
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Signal transducer and activator of transcription 3 in the heart transduces not only a hypertrophic signal but a protective signal against doxorubicin-induced cardiomyopathy2000 · 276 citations
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  3. 3Can the Protective Actions of JAK-STAT in the Heart be Exploited Therapeutically? Parsing the Regulation of Interleukin-6-Type Cytokine Signaling2007 · 78 citations
  4. 4The Role of STATs in Inflammation and Inflammatory Diseases2004 · 166 citations
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