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Stress kinases in the modulation of metabolism and energy balance

Elisa Manieri1, Guadalupe Sabio2

  • 1Myocardial Pathophysiology AreaFundación Centro Nacional de Investigaciones Cardiovasculares Carlos III, CNIC, C/Melchor Fernandez Almagro, 2, 28029 Madrid, SpainDepartment of Immunology and OncologyCentro Nacional de Biotecnología/CSIC, Campus de Cantoblanco, Madrid, Spain Myocardial Pathophysiology AreaFundación Centro Nacional de Investigaciones Cardiovasculares Carlos III, CNIC, C/Melchor Fernandez Almagro, 2, 28029 Madrid, SpainDepartment of Immunology and OncologyCentro Nacional de Biotecnología/CSIC, Campus de Cantoblanco, Madrid, Spain.

Journal of Molecular Endocrinology
|September 13, 2015
PubMed

Insights

Stress-activated protein kinases (SAPK) regulate cellular responses to metabolic stress, potentially contributing to obesity. Further research into SAPK roles in metabolism is crucial for developing new therapies.

Area of Science:

  • Metabolic regulation
  • Obesity research
  • Cellular stress response

Background:

  • Obesity is a global pandemic linked to diabetes, cardiovascular disease, and cancer.
  • Metabolic changes in obesity require understanding underlying mechanisms for new therapies.
  • Stress-activated protein kinases (SAPK) are involved in cellular responses to metabolic stress.

Purpose of the Study:

  • To review the role of SAPKs in metabolism and obesity.
  • To highlight the importance of JNK isoforms, particularly JNK1, in cellular homeostasis and organ crosstalk.
  • To identify gaps in knowledge regarding other JNK isoforms and p38 family members in metabolic regulation.

Main Methods:

  • Literature review of studies on SAPKs, metabolism, and obesity.
  • Analysis of data from tissue-specific knockout models.
  • Synthesis of current understanding of JNK and p38 roles in metabolic pathways.

Main Results:

  • SAPKs, including JNKs and p38, are essential for cellular responses to metabolic stress.
  • JNK isoforms, especially JNK1, play a cell-type-specific role in maintaining homeostasis and organ communication.
  • Evidence suggests SAPKs contribute to the pathogenesis of obesity.

Conclusions:

  • SAPKs are critical regulators of metabolism and may be key targets for obesity therapies.
  • Further investigation into specific JNK isoforms and p38 family members is needed.
  • Understanding SAPK signaling pathways is vital for addressing metabolic dysfunction in obesity.
Keywords:
JNKSAPKadipose tissuebrain and signal transductionmetabolismobesityp38stress

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