Evidence map›Paper›PMID 26469138›Full record

ArticleEndocrinology2016

Deletion of IGF-1 Receptors in Cardiomyocytes Attenuates Cardiac Aging in Male Mice.

Sangmi Ock, Wang Soo Lee, Jihyun Ahn, Hyun Min Kim, Hyun Kang, Ho-Shik Kim, Daewoong Jo, E Dale Abel, Tae Jin Lee, Jaetaek Kim

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
–field-weighted citation impact
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

61 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Obesity accelerates cardiovascular ageing.European heart journal · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Hallmarks of cardiovascular ageing.Nature reviews. Cardiology · 2023
    Review
  18. Article
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Sangmi OckDivision of Endocrinology and Metabolism (S.O., J.A., H.M.K., J.K.), Department of Internal Medicine, Division of Cardiology (W.S.L.), Department of Internal Medicine, and Departments of Anesthesiology (H.K.) and Pathology (T.J.L.), College of Medicine, Chung-Ang University, Seoul, 156-755, Korea; Department of Biochemistry (H.-S.K.), College of Medicine, The Catholic University of Korea, Seoul, 110-758, Korea; Department of Surgery (D.J.), Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism (D.A.), University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.
Wang Soo LeeDivision of Endocrinology and Metabolism (S.O., J.A., H.M.K., J.K.), Department of Internal Medicine, Division of Cardiology (W.S.L.), Department of Internal Medicine, and Departments of Anesthesiology (H.K.) and Pathology (T.J.L.), College of Medicine, Chung-Ang University, Seoul, 156-755, Korea; Department of Biochemistry (H.-S.K.), College of Medicine, The Catholic University of Korea, Seoul, 110-758, Korea; Department of Surgery (D.J.), Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism (D.A.), University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.
Jihyun AhnDivision of Endocrinology and Metabolism (S.O., J.A., H.M.K., J.K.), Department of Internal Medicine, Division of Cardiology (W.S.L.), Department of Internal Medicine, and Departments of Anesthesiology (H.K.) and Pathology (T.J.L.), College of Medicine, Chung-Ang University, Seoul, 156-755, Korea; Department of Biochemistry (H.-S.K.), College of Medicine, The Catholic University of Korea, Seoul, 110-758, Korea; Department of Surgery (D.J.), Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism (D.A.), University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.
Hyun Min KimDivision of Endocrinology and Metabolism (S.O., J.A., H.M.K., J.K.), Department of Internal Medicine, Division of Cardiology (W.S.L.), Department of Internal Medicine, and Departments of Anesthesiology (H.K.) and Pathology (T.J.L.), College of Medicine, Chung-Ang University, Seoul, 156-755, Korea; Department of Biochemistry (H.-S.K.), College of Medicine, The Catholic University of Korea, Seoul, 110-758, Korea; Department of Surgery (D.J.), Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism (D.A.), University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.
Hyun KangDivision of Endocrinology and Metabolism (S.O., J.A., H.M.K., J.K.), Department of Internal Medicine, Division of Cardiology (W.S.L.), Department of Internal Medicine, and Departments of Anesthesiology (H.K.) and Pathology (T.J.L.), College of Medicine, Chung-Ang University, Seoul, 156-755, Korea; Department of Biochemistry (H.-S.K.), College of Medicine, The Catholic University of Korea, Seoul, 110-758, Korea; Department of Surgery (D.J.), Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism (D.A.), University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.
Ho-Shik KimDivision of Endocrinology and Metabolism (S.O., J.A., H.M.K., J.K.), Department of Internal Medicine, Division of Cardiology (W.S.L.), Department of Internal Medicine, and Departments of Anesthesiology (H.K.) and Pathology (T.J.L.), College of Medicine, Chung-Ang University, Seoul, 156-755, Korea; Department of Biochemistry (H.-S.K.), College of Medicine, The Catholic University of Korea, Seoul, 110-758, Korea; Department of Surgery (D.J.), Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism (D.A.), University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.
Daewoong JoDivision of Endocrinology and Metabolism (S.O., J.A., H.M.K., J.K.), Department of Internal Medicine, Division of Cardiology (W.S.L.), Department of Internal Medicine, and Departments of Anesthesiology (H.K.) and Pathology (T.J.L.), College of Medicine, Chung-Ang University, Seoul, 156-755, Korea; Department of Biochemistry (H.-S.K.), College of Medicine, The Catholic University of Korea, Seoul, 110-758, Korea; Department of Surgery (D.J.), Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism (D.A.), University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.
E Dale AbelDivision of Endocrinology and Metabolism (S.O., J.A., H.M.K., J.K.), Department of Internal Medicine, Division of Cardiology (W.S.L.), Department of Internal Medicine, and Departments of Anesthesiology (H.K.) and Pathology (T.J.L.), College of Medicine, Chung-Ang University, Seoul, 156-755, Korea; Department of Biochemistry (H.-S.K.), College of Medicine, The Catholic University of Korea, Seoul, 110-758, Korea; Department of Surgery (D.J.), Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism (D.A.), University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.
Tae Jin LeeDivision of Endocrinology and Metabolism (S.O., J.A., H.M.K., J.K.), Department of Internal Medicine, Division of Cardiology (W.S.L.), Department of Internal Medicine, and Departments of Anesthesiology (H.K.) and Pathology (T.J.L.), College of Medicine, Chung-Ang University, Seoul, 156-755, Korea; Department of Biochemistry (H.-S.K.), College of Medicine, The Catholic University of Korea, Seoul, 110-758, Korea; Department of Surgery (D.J.), Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism (D.A.), University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.
Jaetaek KimDivision of Endocrinology and Metabolism (S.O., J.A., H.M.K., J.K.), Department of Internal Medicine, Division of Cardiology (W.S.L.), Department of Internal Medicine, and Departments of Anesthesiology (H.K.) and Pathology (T.J.L.), College of Medicine, Chung-Ang University, Seoul, 156-755, Korea; Department of Biochemistry (H.-S.K.), College of Medicine, The Catholic University of Korea, Seoul, 110-758, Korea; Department of Surgery (D.J.), Vanderbilt University School of Medicine, Nashville, Tennessee 37232; and Fraternal Order of Eagles Diabetes Research Center and Division of Endocrinology and Metabolism (D.A.), University of Iowa Carver College of Medicine, Iowa City, Iowa 52242.

Funding

Insulin Signaling and the Heart in DiabetesR01DK092065 · NIDDK · UNIVERSITY OF UTAH · PI ABEL, E DALE · 2010 to 2011
$649k
NIDDK NIH HHS R01 DK092065NIDDK NIH HHS R01DK092065
6 · The paper itself

Abstract

IGF-1 receptor (IGF-1R) signaling is implicated in cardiac hypertrophy and longevity. However, the role of IGF-1R in age-related cardiac remodeling is only partially understood. We therefore sought to determine whether the deletion of the IGF-1R in cardiomyocytes might delay the development of aging-associated myocardial pathologies by examining 2-year-old male cardiomyocyte-specific IGF-1R knockout (CIGF1RKO) mice. Aging was associated with the induction of IGF-1R expression in hearts. Cardiomyocytes hypertrophied with age in wild-type (WT) mice. In contrast, the cardiac hypertrophic response associated with aging was blunted in CIGF1RKO mice. Concomitantly, fibrosis was reduced in aged CIGF1RKO compared with aged WT hearts. Expression of proinflammatory cytokines such as IL-1α, IL-1β, IL-6, and receptor activator of nuclear factor-κB ligand was increased in aged WT hearts, but this increase was attenuated in aged CIGF1RKO hearts. Phosphorylation of Akt was increased in aged WT, but not in aged CIGF1RKO, hearts. In cultured cardiomyocytes, IGF-1 induced senescence as demonstrated by increased senescence-associated β-galactosidase staining, and a phosphoinositide 3-kinase inhibitor inhibited this effect. Furthermore, inhibition of phosphoinositide 3-kinase significantly prevented the increase in IL-1α, IL-1β, receptor activator of nuclear factor-κB ligand, and p21 protein expression by IGF-1. These data reveal an essential role for the IGF-1-IGF-1R-Akt pathway in mediating cardiomyocyte senescence.

Indexed as

AgingVentricular RemodelingAnimalsBiomarkersCardiomegalyCells, CulturedCellular SenescenceCytokinesEnzyme InhibitorsFibrosisGene Expression Regulation, DevelopmentalHeart VentriclesInsulin-Like Growth Factor IMaleMice, Inbred C57BLMice, KnockoutAkt1 protein, ratBiomarkersCytokinesEnzyme Inhibitorsinsulin-like growth factor-1, ratInsulin-Like Growth Factor IPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktReceptor, IGF Type 1

Identifiers

PMID26469138
PMCPMC4701888

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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.