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Cited by 879

The DOI matches its OpenAlex record; 7 of the 7 references it cites were found in a registry or an index.

The cardiac phenotype induced by PPARα overexpression mimics that caused by diabetes mellitus

Open access
Brian N. Finck, John J. Lehman, Teresa C. Leone, Michael John Welch, Michael J. Bennett, Attila D Kovács, Xianlin Han, Richard W. Gross, Ray Kozak, Gary D. Lopaschuk, Daniel P. Kelly·2002·Journal of Clinical Investigation
DOI 10.1172/jci14080
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Abstract

Recent evidence has defined an important role for PPARalpha in the transcriptional control of cardiac energy metabolism. To investigate the role of PPARalpha in the genesis of the metabolic and functional derangements of diabetic cardiomyopathy, mice with cardiac-restricted overexpression of PPARalpha (MHC-PPAR) were produced and characterized. The expression of PPARalpha target genes involved in cardiac fatty acid uptake and oxidation pathways was increased in MHC-PPAR mice. Surprisingly, the expression of genes involved in glucose transport and utilization was reciprocally repressed in MHC-PPAR hearts. Consistent with the gene expression profile, myocardial fatty acid oxidation rates were increased and glucose uptake and oxidation decreased in MHC-PPAR mice, a metabolic phenotype strikingly similar to that of the diabetic heart. MHC-PPAR hearts exhibited signatures of diabetic cardiomyopathy including ventricular hypertrophy, activation of gene markers of pathologic hypertrophic growth, and transgene expression-dependent alteration in systolic ventricular dysfunction. These results demonstrate that (a) PPARalpha is a critical regulator of myocardial fatty acid uptake and utilization, (b) activation of cardiac PPARalpha regulatory pathways results in a reciprocal repression of glucose uptake and utilization pathways, and (c) derangements in myocardial energy metabolism typical of the diabetic heart can become maladaptive, leading to cardiomyopathy.

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Cites

Show all 7 references

Research works printed but not linked: 33

  1. Kannel, 1974, Am J Cardiol, 34, 29, 10.1016/0002-9149(74)90089-7 · DOI · Paper page
  2. Rubler, 1972, Am J Cardiol, 30, 595, 10.1016/0002-9149(72)90595-4 · DOI · Paper page
  3. Rodrigues, 1995, J Mol Cell Cardiol, 27, 169, 10.1016/S0022-2828(08)80016-8 · DOI · Paper page
  4. Neely, 1972, Prog Cardiovasc Dis, 15, 289, 10.1016/0033-0620(72)90029-1 · DOI · Paper page
  5. Lopaschuk, 1989, Circ Res, 65, 378, 10.1161/01.RES.65.2.378 · DOI
  6. Murthy, 1977, Diabetes, 26, 222, 10.2337/diabetes.26.3.222 · doi:10.2337/diabetes.26.3.222
  7. Paulson, 1982, Am J Physiol, 242, 1084
  8. Chiu, 2001, J Clin Invest, 107, 813, 10.1172/JCI10947 · DOI · Paper page
  9. Barger, 2000, Trends Cardiovasc Med, 10, 238, 10.1016/S1050-1738(00)00077-3 · DOI · Paper page
  10. Lee, 1995, Mol Cell Biol, 15, 3012, 10.1128/MCB.15.6.3012 · DOI · Paper page
  11. Aoyama, 1998, J Biol Chem, 273, 5678, 10.1074/jbc.273.10.5678 · DOI · Paper page
  12. Leone, 1999, Proc Natl Acad Sci USA, 96, 7473, 10.1073/pnas.96.13.7473 · DOI · Paper page
  13. Kersten, 1999, J Clin Invest, 103, 1489, 10.1172/JCI6223 · DOI · Paper page
  14. Asayama, 1999, Mol Cell Biochem, 194, 227, 10.1023/A:1006930513476 · DOI
  15. Memon, 2000, Endocrinology, 141, 4021, 10.1210/en.141.11.4021 · DOI
  16. Kroetz, 1998, J Biol Chem, 273, 31581, 10.1074/jbc.273.47.31581 · DOI · Paper page
  17. Belke, 1999, Am J Physiol, 277, R1210, 10.1152/ajpcell.1999.277.6.C1210 · DOI · Paper page
  18. Cresci, 1996, Am J Physiol, 270, C1413, 10.1152/ajpcell.1996.270.5.C1413 · DOI
  19. Esser, 1996, J Biol Chem, 271, 6972, 10.1074/jbc.271.12.6972 · DOI
  20. Han, 2001, Anal Biochem, 295, 88, 10.1006/abio.2001.5178 · DOI · Paper page
  21. Young, 2001, FASEB J, 15, 833, 10.1096/fj.00-0351com · DOI · Paper page
  22. Depre, 2000, J Mol Cell Cardiol, 32, 985, 10.1006/jmcc.2000.1139 · DOI · Paper page
  23. Belke, 2000, Am J Physiol, 279, E1104
  24. Wu, 1998, Biochem J, 329, 197, 10.1042/bj3290197 · DOI · Paper page
  25. Ahmed, 1975, Am Heart J, 89, 153, 10.1016/0002-8703(75)90039-3 · DOI · Paper page
  26. Dillmann, 1988, Diabetes Metab Rev, 4, 789, 10.1002/dmr.5610040807 · doi:10.1002/dmr.5610040807
  27. Taegtmeyer, 1997, Am J Cardiol, 80, 3A, 10.1016/S0002-9149(97)00452-9 · DOI
  28. Lewandowski, 1995, Circulation, 91, 2071, 10.1161/01.CIR.91.7.2071 · DOI
  29. McVeigh, 1990, Am J Physiol, 259, H1079
  30. Tian, 2001, Circulation, 103, 2961, 10.1161/01.CIR.103.24.2961 · DOI · Paper page
  31. Frayne, 1993, Curr Opin Lipidol, 4, 197, 10.1097/00041433-199306000-00004 · DOI · Paper page
  32. Kim, 2001, Proc Natl Acad Sci USA, 98, 7522, 10.1073/pnas.121164498 · DOI · Paper page
  33. Wu, 1999, Diabetes, 48, 1593, 10.2337/diabetes.48.8.1593 · DOI · Paper page

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Metadata

Authors
Finck, B. N., Lehman, J. J., Leone, T. C., Welch, M. J., Bennett, M. J., Kovács, A. D., Han, X., Gross, R. W., Kozak, R., Lopaschuk, G. D., & Kelly, D. P.
Venue
Journal of Clinical Investigation
Publisher
American Society for Clinical Investigation
Published
2002-01-01
Volume
109
Issue
1
Pages
121-130
ISSN
0021-9738 (ISSN-L)
DOI
10.1172/jci14080
OpenAlex
W2162919259
Cited by
879
References
7
FWCI
12.53
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: The cardiac phenotype induced by PPARα overexpression mimics that caused by diabetes mellitus. https://app.cochat.ai/papers/10.1172/jci14080
The paper
Finck, B. N., Lehman, J. J., Leone, T. C., Welch, M. J., Bennett, M. J., Kovács, A. D., Han, X., Gross, R. W., Kozak, R., Lopaschuk, G. D., & Kelly, D. P. (2002). The cardiac phenotype induced by PPARα overexpression mimics that caused by diabetes mellitus. Journal of Clinical Investigation. https://doi.org/10.1172/jci14080

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.