Pim-1 kinase inhibits pathological injury by promoting cardioprotective signaling

J Mol Cell Cardiol. 2011 Oct;51(4):554-8. doi: 10.1016/j.yjmcc.2011.01.004. Epub 2011 Jan 19.


Stem cells mediate tissue repair throughout the lifespan of an organism. However, the ability of stem cells to mitigate catastrophic damage, such as that sustained after major myocardial infarction is inadequate to rebuild the heart and restore functional capacity. However, capitalizing on the ability of these cells to attenuate damage in the myocardium, various maneuvers that enhance repair mechanisms to improve cardiac structure and function after injury are being investigated. These studies have led to discovery of various factors that mediate cardioprotection and enhance endogenous repair by 1) salvaging surviving myocardium, 2) promoting homing of stem cells and 3) increasing survival and proliferation of stem cell populations at the site of injury. Herein we report upon a downstream target of Akt kinase, named Pim-1, which promotes cardioprotective signaling and enhances cardiac structure and function after pathological injury. The compilation of studies presented here supports use of Pim-1 to enhance long-term myocardial repair after pathological damage. This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure."

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Proliferation
  • Cell Survival
  • Heart / physiopathology
  • Humans
  • Mice
  • Mice, Transgenic
  • Myocardial Infarction / pathology
  • Myocardial Infarction / physiopathology
  • Myocardial Infarction / therapy
  • Myocardium / enzymology
  • Myocardium / pathology
  • Proto-Oncogene Proteins c-pim-1 / genetics
  • Proto-Oncogene Proteins c-pim-1 / metabolism
  • Proto-Oncogene Proteins c-pim-1 / physiology*
  • Regeneration
  • Signal Transduction*
  • Stem Cell Transplantation
  • Stem Cells / enzymology
  • Stem Cells / physiology


  • Proto-Oncogene Proteins c-pim-1