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Insulin-Like Growth Factor 1 in the Cardiovascular System

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Reviews of Physiology, Biochemistry and Pharmacology, Vol. 175

Abstract

Non-communicable diseases, such as cardiovascular diseases, are the leading cause of mortality worldwide. For this reason, a tremendous effort is being made worldwide to effectively circumvent these afflictions, where insulin-like growth factor 1 (IGF1) is being proposed both as a marker and as a central cornerstone in these diseases, making it an interesting molecule to focus on. Firstly, at the initiation of metabolic deregulation by overfeeding, IGF1 is decreased/inhibited. Secondly, such deficiency seems to be intimately related to the onset of MetS and establishment of vascular derangements leading to atherosclerosis and finally playing a definitive part in cerebrovascular and myocardial accidents, where IGF1 deficiency seems to render these organs vulnerable to oxidative and apoptotic/necrotic damage. Several human cohort correlations together with basic/translational experimental data seem to confirm deep IGF1 implication, albeit with controversy, which might, in part, be given by experimental design leading to blurred result interpretation.

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Acknowledgements

We would like to give a very special thanks to MSc Irene Martín del Estal for her support and to Oliver Gómez Gutierrez, senior medical student at Tecnológico de Monterrey, for his invaluable contribution in figure editing.

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Authors declare to have no competing or financial interests.

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This research did not receive any specific grant from any funding agency in the public, commercial, or not-for-profit sector.

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Correspondence to Inma Castilla-Cortazar .

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Aguirre, G.A., González-Guerra, J.L., Espinosa, L., Castilla-Cortazar, I. (2018). Insulin-Like Growth Factor 1 in the Cardiovascular System. In: Nilius, B., de Tombe, P., Gudermann, T., Jahn, R., Lill, R. (eds) Reviews of Physiology, Biochemistry and Pharmacology, Vol. 175. Reviews of Physiology, Biochemistry and Pharmacology, vol 175. Springer, Cham. https://doi.org/10.1007/112_2017_8

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