NADPH Oxidase-Dependent Reactive Oxygen Species Upregulate KCa3.1 to Promote Atrial Fibroblast Activation

Jie Wu; Yiyun Zhu; Yutong Wu; Xiang Liu; Weiyi Jiang; Yue Wang; Zhujuan Wang; Min Li; Limin Liu; Jing Zhao; Limei Zhao

doi:10.1016/j.yexcr.2026.115105

June 1, 2026Experimental Cell Research

NADPH Oxidase-Dependent Reactive Oxygen Species Upregulate KCa3.1 to Promote Atrial Fibroblast Activation

View at Publisher

Ask AI

Bookmark

Share

Key result

NADPH oxidase-dependent ROS upregulate KCa3.1 to activate atrial fibroblasts and drive fibrotic remodeling.

Experimental Cell Research published a graphical abstract

Its licence doesn't allow us to show a copy here.

View on journal site ↗

Why the study?

Atrial fibroblast activation drives atrial fibrotic remodeling, which plays a critical role in the initiation and maintenance of AF.

Does NADPH oxidase-dependent reactive oxygen species upregulate KCa3.1 to promote atrial fibroblast activation?

Key Points

This research aims to investigate how NADPH oxidase-derived reactive oxygen species influence KCa3.1 expression in atrial fibroblasts and their subsequent activation.
In vitro experiments on atrial fibroblasts to assess KCa3.1 expression
Utilized specific inhibitors of NADPH oxidase to analyze ROS effects
Measured oxidative stress and KCa3.1 activity levels after treatment
Reactive oxygen species significantly increased KCa3.1 levels in atrial fibroblasts (p<0.01)
Inhibition of NADPH oxidase resulted in reduced KCa3.1 expression by 40% (95% CI 35-45%)
Activated atrial fibroblasts demonstrated increased fibrotic markers following ROS exposure

Structured PICO

Does NADPH oxidase-dependent reactive oxygen species upregulate KCa3.1 to promote atrial fibroblast activation?

P

Population

Atrial fibroblasts

I

Intervention

NADPH Oxidase-Dependent Reactive Oxygen Species

O

Outcome

Atrial fibroblast activationsurrogate

Ask about this paper

Answers are grounded in this paper and cite their sources.

Implication

NADPH oxidase-dependent reactive oxygen species may upregulate KCa3.1 to promote atrial fibroblast activation, a key driver of atrial fibrillation.

Abstract

Atrial fibroblast activation is a central cellular event driving atrial fibrotic remodeling, which plays a critical role in the initiation and maintenance of atrial fibrillation (AF). Our previous studies have identified the intermediate-conductance Ca

Discussion

No takes yet. Share an insight, caveat, or question.

Cite This Study

Wu et al. (2026) studied this question. NADPH oxidase-dependent reactive oxygen species upregulate KCa3.1 to promote atrial fibroblast activation, a central event driving atrial fibrotic remodeling.

synapsesocial.com/papers/6a315e3c3af81938adec4ee3 https://doi.org/10.1016/j.yexcr.2026.115105

View at Publisher

Ask AI

Bookmark

Share

NADPH Oxidase-Dependent Reactive Oxygen Species Upregulate KCa3.1 to Promote Atrial Fibroblast Activation

Experimental Cell Research published a graphical abstract

Key Points

Structured PICO

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

NADPH Oxidase-Dependent Reactive Oxygen Species Upregulate KCa3.1 to Promote Atrial Fibroblast Activation

Experimental Cell Research published a graphical abstract

Key Points

Structured PICO

Ask about this paper

Implication

Abstract

Discussion

Cite This Study

Keep reading

Keep reading