ArticleOxidative medicine and cellular longevity2022
Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- 4E-BP inhibition ameliorates heart failure through translational upregulation of SERCA2a and modulation of mitochondrial redox signaling in cardiomyocytes.Redox biology · 2026Article
- Cardiac remodeling pathways do not accelerate disease onset and severity in a mouse model of PLN-R14del cardiomyopathy.Scientific reports · 2025Article
- Traditional Chinese medicine as a protective strategy against chemotherapy-induced cardiotoxicity: An overview of the literature.Journal of traditional and complementary medicine · 2025Review
- Guanxinning tablets improve myocardial hypertrophy by inhibiting the activation of MEK-ERK1/2 signaling pathway.Journal of applied biomedicine · 2023Article
- Selenoprotein P, Peroxiredoxin-5, Renalase and Selected Cardiovascular Consequences Tested in Ambulatory Blood Pressure Monitoring and Echocardiography.Antioxidants (Basel, Switzerland) · 2023Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
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Abstract
A recent study showed that peroxiredoxins (Prxs) play an important role in the development of pathological cardiac hypertrophy. However, the involvement of Prx5 in cardiac hypertrophy remains unclear. Therefore, this study is aimed at investigating the role and mechanisms of Prx5 in pathological cardiac hypertrophy and dysfunction. Transverse aortic constriction (TAC) surgery was performed to establish a pressure overload-induced cardiac hypertrophy model. In this study, we found that Prx5 expression was upregulated in hypertrophic hearts and cardiomyocytes. In addition, Prx5 knockdown accelerated pressure overload-induced cardiac hypertrophy and dysfunction in mice by activating oxidative stress and cardiomyocyte apoptosis. Importantly, heart deterioration caused by Prx5 knockdown was related to mitogen-activated protein kinase (MAPK) pathway activation. These findings suggest that Prx5 could be a novel target for treating cardiac hypertrophy and heart failure.
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