Asociación entre el sistema IGF y PAPP-A en ateroesclerosis coronaria

Abstract

Atherosclerosis is a condition that involves multiple pathophysiological mechanisms and whose knowledge has not been fully elucidated. Often, scientific advances on the atherogenic pathophysiology generate that molecules not previously considered in the scene of this disease, were attributed actions on the onset or progression of it. A representative example is the study of a new mechanism involved in the atherogenic process, consisting of the association between the insulin-like growth factor (IGF) system and pregnancy-associated plasma protein-A (PAPP-A). Insulin-like growth factor system is a family of peptides that include 3 peptide hormones, 4 transmembrane receptors and 6 binding proteins. Insulin-like growth factor-1 (IGF-1) is the main ligand of the IGF system involved in coronary atherosclerosis. IGF-1 exerts its effects via activation of the IGF-1R receptor on vascular smooth muscle cells or macrophages. In vascular smooth muscle cells promotes migration and prevents apoptosis which increases plaque stability while in macrophages reduces reverse cholesterol transport leading to the formation of foam cells. Regulation of IGF-1 endothelial bioavailability is carried out by IGFBP proteases, mainly by PAPP-A. In this review, we address the mechanisms between IGF system and PAPP-A in atherosclerosis with emphasis on molecular effects on vascular smooth muscle cells and macrophages.

Evaluating the predictive efficacy of first trimester biochemical markers (PAPP-A, fβ-hCG) in forecasting preterm delivery incidences

“…Outside the realm of pregnancy, PAPP-A has been investigated for its association with cardiovascular risk, underscoring its broad relevance to human health 13 . The literature describes its involvement in a variety of physiological and pathological processes, including metabolism, cancer, and neurodegenerative diseases 14 .…”

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“…33 The possible reason could be that local IGF-I in coronary atherosclerosis stimulates vascular smooth muscle cell proliferation and releases inflammatory factors leading to vulnerable plaques. 34,35 Due to the complexity of IGF system function, clinical implications vary in different disease populations.…”

“… 33 The possible reason could be that local IGF-I in coronary atherosclerosis stimulates vascular smooth muscle cell proliferation and releases inflammatory factors leading to vulnerable plaques. 34 , 35 Due to the complexity of IGF system function, clinical implications vary in different disease populations. A large prospective study found that the association between free IGF-I and T2DM varied by insulin levels, 36 and indicated an inverse association limited to subjects with higher levels of insulin.…”