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Dual inhibition of Mst1 and Mst2 exacerbates cardiac dysfunction during pressure overload stress in mice

Jin Guan1, Nadezhda Fefelova1, Peiyong Zhai1

  • 1Department of Cell Biology and Molecular Medicine, Cardiovascular Research Institute, Rutgers New Jersey Medical School, USA.

Journal of Molecular and Cellular Cardiology
|February 1, 2025
PubMed

Insights

Mst1/2 kinases protect adult hearts from stress by maintaining cardiomyocyte maturity. Loss of Mst1/2 function in stressed hearts promotes dedifferentiation and dysfunction.

Area of Science:

  • Cardiovascular Biology
  • Molecular Signaling
  • Cellular Stress Response

Background:

  • Heart failure is a major global health burden.
  • The Hippo-Yap pathway regulates cardiac stress responses.
  • The role of core Hippo kinases Mst1/2 in stressed adult cardiomyocytes is unclear.

Purpose of the Study:

  • Investigate the function of Mst1 and Mst2 kinases in adult cardiomyocytes under chronic stress.
  • Determine the impact of Mst1/2 loss on cardiac function and cellular phenotypes during stress.

Main Methods:

  • Utilized genetic mouse models with Mst1/2 gene deletion in cardiomyocytes.
  • Analyzed cardiac function and cellular markers in response to induced stress.
  • Examined Yap-TEAD1 activation, cell cycling, and cardiomyocyte differentiation status.

Main Results:

  • Mst1/2 inhibition had opposing effects on stress-induced cardiac dysfunction depending on the extent of inhibition.
  • Loss of Mst1/2 in stressed hearts enhanced Yap-TEAD1 activation and cell cycling.
  • Mst1/2 deficiency led to cardiomyocyte dedifferentiation, impairing contractile function.

Conclusions:

  • Mst1/2 kinases play a crucial role in maintaining cardiomyocyte maturity in the adult heart.
  • Mst1/2 signaling acts as a protective mechanism against stress-induced cardiac dysfunction.
  • Targeting Mst1/2 may offer therapeutic strategies for heart failure.

Keywords:
Cardiac hypertrophyCardiomyocyteCardiovascular diseaseHeart failureHippo-YapSignal transduction

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