The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Minimally invasive aortic banding in mice: effects of altered cardiomyocyte insulin signaling during pressure overload
Abstract
We developed a minimally invasive method for producing left ventricular (LV) pressure overload in mice. With the use of this technique, we quickly and reproducibly banded the transverse aorta with low surgical morbidity and mortality. Minimally invasive transverse aortic banding (MTAB) acutely and chronically increased LV systolic pressure, increased heart weight-to-body weight ratio, and induced myocardial fibrosis. We used this technique to determine whether reduced insulin signaling in the heart altered the cardiac response to pressure overload. Mice with cardiac myocyte-restricted knockout of the insulin receptor (CIRKO) have smaller hearts than wild-type (WT) controls. Four weeks after MTAB, WT and CIRKO mice had comparably increased LV systolic pressure, increased cardiac mass, and induction of mRNA for β-myosin heavy chain and atrial natriuretic factor. However, CIRKO hearts were more dilated, had depressed LV systolic function by echocardiography, and had greater interstitial fibrosis than WT mice. Expression of connective tissue growth factor was increased in banded CIRKO hearts compared with WT hearts. Thus lack of insulin signaling in the heart accelerates the transition to a more decompensated state during cardiac pressure overload. The use of the MTAB approach should facilitate the study of the pathophysiology and treatment of pressure-overload hypertrophy.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Insulin receptor-deficient hearts also have increased susceptibility to injury when exposed to hypertrophic stimuli such as pressure overload and chronic adrenergic stimulation with isoproterenol (150, 231).”
From Cardiac remodeling in obesity (2008) · cites this paper as [150]
Citations
Cites
1 retracted
Rockman, H. A., Ross, R. S., Harris, A. N., Knowlton, K. U., Steinhelper, M. E., Field, L. J., Ross, J., & Chien, K. R. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.18.8277 · Cited by 807
RetractedReaven, G. M., Lithell, H., & Landsberg, L. (1996) · New England Journal of Medicine · doi:10.1056/nejm199602083340607 · Cited by 1,435
Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans.
Anderson, E. A., Hoffman, R. P., Balon, T. W., Sinkey, C. A., & Mark, A. L. (1991) · Journal of Clinical Investigation · doi:10.1172/jci115260 · Cited by 1,075
Impact of Diabetes on Cardiac Structure and Function
Devereux, R. B., Roman, M. J., Paranicas, M., O’Grady, M. J., Lee, E. T., Welty, T. K., Fabsitz, R. R., Robbins, D. C., Rhoades, E. R., & Howard, B. V. (2000) · Circulation · doi:10.1161/01.cir.101.19.2271 · Cited by 943
IRS proteins and the common path to diabetes
White, M. F. (2002) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00514.2001 · Cited by 925
The MEK1–ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice
Bueno, O. F., Windt, L. J. D., Tymitz, K. M., Witt, S. A., Kimball, T. R., Klevitsky, R., Hewett, T. E., Jones, S. P., Lefer, D. J., Peng, C., et al. (2000) · The EMBO Journal · doi:10.1093/emboj/19.23.6341 · Cited by 774
Cytoplasmic Signaling Pathways That Regulate Cardiac Hypertrophy
Molkentin, J. D., & Dorn, G. W. (2001) · Annual Review of Physiology · doi:10.1146/annurev.physiol.63.1.391 · Cited by 684
The conserved phosphoinositide 3‐kinase pathway determines heart size in mice
Shioi, T., Kang, P., Douglas, P., Hampe, J., Yballe, C., Lawitts, J., Cantley, L., & Izumo, S. (2000) · EMBO Journal · doi:10.1093/emboj/19.11.2537 · Cited by 646
Contribution of oxidative metabolism and glycolysis to ATP production in hypertrophied hearts
Allard, M., Schönekess, B. O., Henning, S. L., English, D. R., & Lopaschuk, G. D. (1994) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1994.267.2.h742 · Cited by 576
Regulation of Myocardial Contractility and Cell Size by Distinct PI3K-PTEN Signaling Pathways
Crackower, M. A., Oudit, G. Y., Kozieradzki, I., Sarao, R., Sun, H., Sasaki, T., Hirsch, E., Suzuki, A., Shioi, T., Irie-Sasaki, J., et al. (2002) · Cell · doi:10.1016/s0092-8674(02)00969-8 · Cited by 576
Cited by
Sorted by citations
Shiojima, I. (2005) · Journal of Clinical Investigation · doi:10.1172/jci24682 · Cited by 935
Cardiovascular Actions of Insulin
Muniyappa, R., Montagnani, M., Koh, K. K., & Quon, M. J. (2007) · Endocrine Reviews · doi:10.1210/er.2007-0006 · Cited by 888
Abel, E. D., Litwin, S. E., & Sweeney, G. (2008) · Physiological Reviews · doi:10.1152/physrev.00017.2007 · Cited by 736
Self-citationPoornima, I. G., Parikh, P., & Shannon, R. P. (2006) · Circulation Research · doi:10.1161/01.res.0000207406.94146.c2 · Cited by 567
Buchanan, J., Mazumder, P. K., Hu, P., Chakrabarti, G., Roberts, M. W., Yun, U. J., Cooksey, R. C., Litwin, S. E., & Abel, E. D. (2005) · Endocrinology · doi:10.1210/en.2005-0938 · Cited by 555
Self-citation
Metadata
- Authors
- Hu, P., Zhang, D., Swenson, L., Chakrabarti, G., Abel, E. D., & Litwin, S. E.
- Affiliations
- University of Utah (US)
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2003-09
- Volume
- 285
- Issue
- 3
- Pages
- H1261-H1269
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2153616813
- Cited by
- 245
- References
- 44
- Citations by year
- 2026: 6 · 2025: 8 · 2024: 8 · 2023: 6 · 2022: 10 · 2021: 11 · 2020: 8 · 2019: 9 · 2018: 8 · 2017: 14 · 2016: 10 · 2015: 16 · 2014: 10 · 2013: 17 · 2012: 16
- FWCI
- 4.39
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r03dk058073-03)
- U.S. Public Health Service (U01-70525)
- National Heart, Lung, and Blood Institute (T32-HL-7576, HL-52338-06, P50HL052338, T32HL007576)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK58073, R01DK092065)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Keywords
- left ventricular pressure overload, cardiac hypertrophy, myocardial fibrosis, connective tissue growth factor, beta-myosin heavy chain, atrial natriuretic peptide, cardiac remodeling, heart failure
- MeSH terms
- Animals, Aorta, Blood Pressure, Disease Models, Animal, Fibrosis, Insulin, Male, Mice, Inbred C57BL, Myocardial Contraction, Signal Transduction, Hypertrophy, Left Ventricular, Ventricular Pressure, Myocytes, Cardiac, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
