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January 15, 2015CirculationOpen Access

NADPH Oxidase 4 Induces Cardiac Fibrosis and Hypertrophy Through Activating Akt/mTOR and NFκB Signaling Pathways

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Key result

Cardiac-specific Nox4 overexpression in mice led to an ≈10-fold increase in Nox4 protein and an 8-fold increase in reactive oxygen species, causing cardiac fibrosis and hypertrophy.

Why the study?

Does Nox4 upregulation induce cardiac remodeling and does Nox4 inhibition with GKT137831 attenuate it in a transgenic mouse model?

Population

Cardiac-specific human Nox4 transgenic mice and control mice

Comparison

Angiotensin II infusion and/or treatment with… vs Control mice without AngII infusion or transgene

Design

Preclinical

Authors

QZQingwei ZhaoThe University of Texas Health Science Center at San AntonioSVSuryavathi ViswanadhapalliTexas A&M University – San AntonioPWPaul J. WilliamsUniversity of the West Indies System

Discussion

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Member takes

Overview

Nox4 inhibition may merit testing for remodeling; leaves open translation from mouse overexpression to clinical use.

Structured PICO

Does Nox4 upregulation induce cardiac remodeling and does Nox4 inhibition with GKT137831 attenuate it in a transgenic mouse model?

P
Population
Cardiac-specific human Nox4 transgenic mice and control littermates studied to investigate the role of Nox4 in cardiac remodeling.
I
Intervention
Angiotensin II (AngII) infusion and/or treatment with GKT137831 (a Nox4/Nox1 inhibitor)
C
Comparator
Control mice without AngII infusion or transgene
O
Outcome
Cardiac remodeling (fibrosis and hypertrophy), oxidative stress, and activation of Akt-mTOR and NFκB signaling pathwayssurrogate

Nox4 upregulation drives cardiac fibrosis and hypertrophy via Akt-mTOR and NFκB pathways, highlighting Nox4 inhibition as a potential therapeutic strategy for cardiac remodeling.

Cite This Study

Zhao et al. (2015) studied Cardiac remodeling. Nox4 overexpression (c-hNox4Tg) and Angiotensin II infusion vs. Control mice was evaluated on Cardiac remodeling (fibrosis and hypertrophy). Cardiac-specific Nox4 overexpression in mice led to an ≈10-fold increase in Nox4 protein and an 8-fold increase in reactive oxygen species, causing cardiac fibrosis and hypertrophy.

synapsesocial.com/papers/6a88153b4c82be800eeb4162https://doi.org/10.1161/circulationaha.114.011079
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Also Consider

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

  1. 1Endothelial NADPH Oxidase 4 Protects Against Angiotensin II-Induced Cardiac Fibrosis and Inflammation2021 · 24 citations
  2. 2The Nox1/4 Dual Inhibitor GKT137831 or Nox4 Knockdown Inhibits Angiotensin‐II‐Induced Adult Mouse Cardiac Fibroblast Proliferation and Migration. AT1 Physically Associates With Nox42015 · 72 citations
  3. 3NADPH oxidase-4 promotes eccentric cardiac hypertrophy in response to volume overload2019 · 31 citations
  4. 4NAD(P)H Oxidase 4 Mediates Transforming Growth Factor-β1–Induced Differentiation of Cardiac Fibroblasts Into Myofibroblasts2005 · 788 citations
  5. 5NADPH Oxidase-4 Driven Cardiac Macrophage Polarization Protects Against Myocardial Infarction–Induced Remodeling2017 · 48 citations