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<p>Cardiac fibrosis results from cardiovascular diseases (CVDs) and is characterized by excessive extracellular matrix (ECM) accumulation, particularly collagen, leading to cardiac dysfunction. Despite the availability of treatments for CVDs, no targeted therapies are available to prevent disease progression to irreversible stages. Further research is needed to explore the pathways and signaling molecules involved in this progression. The renin-angiotensin system (RAS) plays a significant role, with pharmacological agents targeting its harmful axis, i.e., Angiotensin-converting enzyme (ACE)/Angiotensin II (Ang II)/Angiotensin 1 receptor (AT1R) axis, while an antagonistic axis, ACE2/Angiotensin 1–7 (Ang 1–7)/mitochondrial assembly receptor (MasR) axis offers cardioprotective effects. Reactive oxygen species (ROS) also contribute to CVDs, with NADPH oxidases (NOXes) being key inducers of ROS. NOX1, NOX2, NOX4, and NOX5 are upregulated in pathological conditions, exacerbating the disease. This review focuses on the mechanisms by which the ACE/Ang II/AT1R and ACE2/Ang 1–7/MasR axes regulate NOX activity, aiming to enhance our understanding of future targeted therapies.</p>

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Unraveling the interplay between RAS axes and NOX signaling in fibroblasts during cardiac fibrosis

  • 期刊论文

  • 发表日期：

    2025年10月4日

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  • Gauri Chaturvedi,
  • Anita Chauhan,
  • Nandini Dubey,
  • Sandeep Seth,
  • Jagriti Bhatia,
  • Subhash Chandra Yadav,
  • Harlokesh Narayan Yadav

摘要

Cardiac fibrosis results from cardiovascular diseases (CVDs) and is characterized by excessive extracellular matrix (ECM) accumulation, particularly collagen, leading to cardiac dysfunction. Despite the availability of treatments for CVDs, no targeted therapies are available to prevent disease progression to irreversible stages. Further research is needed to explore the pathways and signaling molecules involved in this progression. The renin-angiotensin system (RAS) plays a significant role, with pharmacological agents targeting its harmful axis, i.e., Angiotensin-converting enzyme (ACE)/Angiotensin II (Ang II)/Angiotensin 1 receptor (AT1R) axis, while an antagonistic axis, ACE2/Angiotensin 1–7 (Ang 1–7)/mitochondrial assembly receptor (MasR) axis offers cardioprotective effects. Reactive oxygen species (ROS) also contribute to CVDs, with NADPH oxidases (NOXes) being key inducers of ROS. NOX1, NOX2, NOX4, and NOX5 are upregulated in pathological conditions, exacerbating the disease. This review focuses on the mechanisms by which the ACE/Ang II/AT1R and ACE2/Ang 1–7/MasR axes regulate NOX activity, aiming to enhance our understanding of future targeted therapies.