The DOI matches its Crossref record; 161 of the 161 references it cites were found in a registry or an index.
Insulin signalling in the heart
Abstract
The main role of insulin in the heart under physiological conditions is obviously the regulation of substrate utilization. Indeed, insulin promotes glucose uptake and its utilization via glycolysis. In addition, insulin participates in the regulation of long-chain fatty acid uptake, protein synthesis, and vascular tonicity. Significant advancements have been made over the last 20 years in the understanding of the signal transduction elements involved in these insulin effects. Among these molecular mechanisms, the phosphatidylinositol 3-kinase/protein kinase B (Akt) pathway is thought to play a crucial role. Under pathological conditions, such as type-2 diabetes, myocardial ischaemia, and cardiac hypertrophy, insulin signal transduction pathways and action are clearly modified. These molecular signalling alterations are often linked to atypical crosstalks with other signal transduction pathways. On the other hand, pharmacological modifications of parallel and interdependent signalling components, such as the AMP-activated protein kinase pathway, are now considered to be a good therapeutic approach to treat insulin-signalling defects such as insulin resistance and type-2 diabetes. In this review, we will focus on the description of the molecular signalling elements involved in insulin action in the heart and vasculature under these different physiological, pathological, and therapeutical conditions.
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1 retracted
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Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor
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Insulin signalling and the regulation of glucose and lipid metabolism
Saltiel, A. R., & Kahn, C. R. (2001) · Nature · doi:10.1038/414799a · Cited by 5,326
Randle, P. J., Garland, P. B., Hales, C. N., & Newsholme, E. A. (1963) · The Lancet · doi:10.1016/s0140-6736(63)91500-9 · Cited by 5,093
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TSC2 Mediates Cellular Energy Response to Control Cell Growth and Survival
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Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation
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TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling
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Cited by
Tan, Y., Zhang, Z., Zheng, C., Wintergerst, K. A., Keller, B. B., & Cai, L. (2020) · Nature Reviews Cardiology · doi:10.1038/s41569-020-0339-2 · Cited by 835
AMPK inhibition in health and disease
Viollet, B., Horman, S., Leclerc, J., Lantier, L., Foretz, M., Billaud, M., Giri, S., & Andreelli, F. (2010) · Critical Reviews in Biochemistry and Molecular Biology · doi:10.3109/10409238.2010.488215 · Cited by 383
Self-citationHepatic Autophagy Is Suppressed in the Presence of Insulin Resistance and Hyperinsulinemia
Liu, H.-Y., Han, J., Cao, S. Y., Hong, T., Zhuo, D., Shi, J., Liu, Z., & Cao, W. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.033936 · Cited by 352
Insulin Resistance and Heart Failure
Aroor, A. R., Mandavia, C. H., & Sowers, J. R. (2012) · Heart Failure Clinics · doi:10.1016/j.hfc.2012.06.005 · Cited by 252
Turdi, S., Kandadi, M. R., Zhao, J., Huff, A. F., Du, M., & Ren, J. (2011) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2010.12.007 · Cited by 103
Metadata
- Authors
- Bertrand, L., Horman, S., Beauloye, C., & Vanoverschelde, J.-L.
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2008-04-30
- Volume
- 79
- Issue
- 2
- Pages
- 238-248
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W1972142752
- Cited by
- 270
- References
- 161
- FWCI
- 5.71
- Type
- journal article
- Language
- en
- Open access
- closed
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- Bertrand, L., Horman, S., Beauloye, C., & Vanoverschelde, J.-L. (2008). Insulin signalling in the heart. Cardiovascular Research. https://doi.org/10.1093/cvr/cvn093
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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