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Unmasking Protein Phosphatase 2A Regulatory Subunit B as a Crucial Factor in the Progression of Dilated Cardiomyopathy. | LitMetric

AI Article Synopsis

  • Dilated cardiomyopathy (DCM) is a leading cause of heart failure, and while progress has been made in understanding it, more research is needed on diagnostic and treatment options.
  • The study found that a specific protein's mRNA levels were altered in DCM patients, and its knockdown in heart cells led to increased reactive oxygen species and decreased ATP production, worsening heart function in a mouse model.
  • The research highlighted that this protein impacts the STAT3 signaling pathway, affecting inflammation and mitochondrial function, suggesting it could be a potential target for DCM therapy.

Article Abstract

Dilated cardiomyopathy (DCM) is one of the major causes of heart failure. Although significant progress has been made in elucidating the underlying mechanisms, further investigation is required for clarifying molecular diagnostic and therapeutic targets. In this study, we found that the mRNA level of protein phosphatase 2 regulatory subunit B' delta () was altered in the peripheral blood plasma of DCM patients. Knockdown of in murine cardiomyocytes increased the intracellular levels of reactive oxygen species (ROS) and inhibited adenosine triphosphate (ATP) synthesis. In vivo knockdown of in an isoproterenol (ISO)-induced DCM mouse model aggravated the pathogenesis and ultimately led to heart failure. Mechanistically, -deficient cardiomyocytes showed an increase in phosphorylation of STAT3 at Y705 and a decrease in phosphorylation of STAT3 at S727. The elevated levels of phosphorylation at Y705 in STAT3 triggered the upregulation of interleukin 6 (IL6) expression. Moreover, the decreased phosphorylation at S727 in STAT3 disrupted mitochondrial electron transport chain function and dysregulated ATP synthesis and ROS levels. These results hereby reveal a novel role for in modulating STAT3 pathway in DCM, suggesting it as a potential target for the therapy of the disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11352103PMC
http://dx.doi.org/10.3390/biomedicines12081887DOI Listing

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