JNK and cardiometabolic dysfunction

Siobhan M Craige1,2, Kai Chen3, Robert M Blanton4

  • 1Division of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA 01605, U.S.A.

Bioscience Reports
|July 5, 2019
PubMed

Insights

Cardiometabolic syndrome (CMS), a growing global health issue, involves metabolic and cardiovascular diseases. This review explores how c-Jun N-terminal Kinases (JNK) signaling impacts CMS, suggesting JNK as a potential therapeutic target.

Area of Science:

  • Biomedical Science
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Cardiometabolic syndrome (CMS) is a complex cluster of diseases including impaired glucose tolerance, obesity, dyslipidemia, and hypertension.
  • CMS affects over 25% of the global population and significantly increases the risk of cardiovascular diseases like atherosclerosis and myocardial infarction.
  • Understanding the molecular signaling pathways underlying CMS is crucial for developing effective treatments.

Purpose of the Study:

  • To review the in vivo implications of c-Jun N-terminal Kinases (JNK) signaling in Cardiometabolic Syndrome (CMS).
  • To evaluate the potential of targeting JNK pathways as a therapeutic strategy for CMS.
  • To highlight the importance of JNK pathway research given the complexity and rising prevalence of CMS.

Main Methods:

  • Literature review focusing on in vivo studies of JNK signaling in relation to CMS components.
  • Analysis of current research on the role of JNK pathways in metabolic and cardiovascular dysregulation.
  • Synthesis of findings to assess JNK as a therapeutic target.

Main Results:

  • JNK signaling pathways have been implicated in the development and progression of various CMS conditions.
  • Evidence suggests that modulating JNK activity could impact multiple facets of CMS.
  • The complexity of CMS necessitates a detailed understanding of JNK's role across different tissues.

Conclusions:

  • JNK signaling is a relevant target for therapeutic intervention in Cardiometabolic Syndrome.
  • Further research into the specific roles of JNK pathways in vivo is warranted.
  • Targeting JNK may offer a strategy for addressing the multifaceted nature of CMS.

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