Evidence map›Paper›PMID 21255581›Full record

ReviewJournal of molecular and cellular cardiology2011

Pim-1 kinase inhibits pathological injury by promoting cardioprotective signaling.

Kimberlee M Fischer, Christopher T Cottage, Mathias H Konstandin, Mirko Völkers, Mohsin Khan, Mark A Sussman

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.6field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Adult Cardiac Stem Cell Aging: A Reversible Stochastic Phenomenon?Oxidative medicine and cellular longevity · 2019
    Review
  10. Article
  11. Pim-1 Kinase Phosphorylates Cardiac Troponin I and Regulates Cardiac Myofilament Function.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018
    Article
  12. Decline in cellular function of aged mouse c-kitThe Journal of physiology · 2017
    Article
  13. Article
  14. Pim1 Kinase Overexpression Enhances ckitJournal of the American College of Cardiology · 2016
    Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Cardiac stem cells: biology and clinical applications.Antioxidants & redox signaling · 2014
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Kimberlee M FischerSan Diego State Heart Institute, San Diego State University, San Diego, CA 92182, USA.
Christopher T Cottage
Mathias H Konstandin
Mirko Völkers
Mohsin Khan
Mark A Sussman
San Diego State University · US

Funding

Surgery, Physiology and ImmunohistopathologyP01HL085577 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI GUSTAFSSON, ASA B. · 2006 to 2017
$18.4M
Stem Cell Signaling in the Pathologically Challenged MyocardiumR37HL091102 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2008 to 2017
$3.8M
Antagonism of myocardial aging and senescence with Pim-1 kinaseR01HL105759 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2011 to 2015
$1.8M
Nucleolar disruption in response to cardiomyopathic stress and injuryR21HL102714 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2010 to 2011
$411k
Inducible Notch improves progenitor cell repair of damaged heartR21HL104544 · NHLBI · SAN DIEGO STATE UNIVERSITY · PI SUSSMAN, MARK ALAN · 2010 to 2011
$411k
NHLBI NIH HHS P01 HL085577NHLBI NIH HHS R01 HL105759NHLBI NIH HHS R21 HL102714NHLBI NIH HHS R21 HL104544NHLBI NIH HHS R37 HL091102
6 · The paper itself

Abstract

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."

Indexed as

Signal TransductionAnimalsCell ProliferationCell SurvivalHeartHumansMiceMice, TransgenicMyocardial InfarctionMyocardiumProto-Oncogene Proteins c-pim-1RegenerationStem CellsStem Cell TransplantationProto-Oncogene Proteins c-pim-1

Identifiers

PMID21255581
PMCPMC3130822
OpenAlexW2049584647

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.