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LKB1 suppression promotes cardiomyocyte regeneration via LKB1-AMPK-YAP axis

Shuang Qu1, Qiao Liao1, Cheng Yu1

  • 1Department of Cardiology, Daping Hospital, The Third Military Medical University, Chongqing, China; Chongqing Key Laboratory for Hypertension Research, Chongqing Cardiovascular Clinical Research Center, Chongqing Institute of Cardiology, Chongqing, China.

Bosnian Journal of Basic Medical Sciences
|May 1, 2022
PubMed

Insights

Liver kinase B1 (LKB1) inhibits cardiomyocyte proliferation by activating AMP-activated protein kinase (AMPK), which regulates Yes-associated protein (YAP). This LKB1-AMPK-YAP axis offers a target for cardiac regeneration.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Regenerative Medicine

Background:

  • Limited regenerative capacity of cardiomyocytes in adult mammals.
  • AMP-activated protein kinase (AMPK) suppresses cardiomyocyte proliferation.
  • The role of upstream kinase liver kinase B1 (LKB1) in this process remains unclear.

Purpose of the Study:

  • To investigate the role of LKB1 in cardiomyocyte proliferation.
  • To elucidate the molecular mechanisms linking LKB1 to cardiomyocyte proliferation.
  • To identify potential therapeutic targets for cardiac regeneration.

Main Methods:

  • Loss- and gain-of-function studies of LKB1 in cardiomyocytes.
  • High-throughput RNA sequencing to identify downstream effectors.
  • Assessment of AMPK activity and YAP nuclear translocation.

Main Results:

  • LKB1 levels increase postnatally and negatively correlate with cardiomyocyte proliferation.
  • Yes-associated protein (YAP) identified as a downstream effector of LKB1.
  • AMPK is essential for LKB1 knockdown-induced proliferation and mediates LKB1's regulation of YAP.

Conclusions:

  • The LKB1-AMPK-YAP signaling axis regulates cardiomyocyte proliferation.
  • LKB1 inactivation promotes proliferation via AMPK-mediated YAP regulation.
  • Targeting the LKB1-AMPK-YAP pathway may enhance cardiac regeneration.

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