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Updated: Mar 25, 2026
In Vitro Model of Coronary Angiogenesis
Published on: March 10, 2020
[Association between IGF system and PAPP-A in coronary atherosclerosis]
Alfonso Eduardo Fierro-Macías1, Esaú Floriano-Sánchez2, Victoria Michelle Mena-Burciaga1
1Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, México, DF, México.
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.
Insights
The insulin-like growth factor (IGF) system and pregnancy-associated plasma protein-A (PAPP-A) play key roles in atherosclerosis. This review details their molecular mechanisms in vascular smooth muscle cells and macrophages, impacting plaque stability and foam cell formation.
Area of Science:
- Cardiovascular Biology
- Endocrinology
- Molecular Medicine
Background:
- Atherosclerosis involves complex, incompletely understood pathophysiological mechanisms.
- New molecular players are continually identified in atherogenesis.
- The insulin-like growth factor (IGF) system and its regulators are implicated in cardiovascular disease.
Purpose of the Study:
- To review the interplay between the IGF system and pregnancy-associated plasma protein-A (PAPP-A) in atherosclerosis.
- To elucidate the molecular mechanisms of IGF-1 and PAPP-A in vascular cells.
- To highlight their roles in atherogenic processes.
Main Methods:
- Literature review focusing on the IGF system, PAPP-A, and atherosclerosis.
- Analysis of molecular effects on vascular smooth muscle cells and macrophages.
- Emphasis on IGF-1 signaling pathways and PAPP-A's regulatory role.
Main Results:
- IGF-1 influences vascular smooth muscle cells by promoting migration and preventing apoptosis, enhancing plaque stability.
- In macrophages, IGF-1 reduces reverse cholesterol transport, contributing to foam cell formation.
- PAPP-A regulates IGF-1 bioavailability, modulating these cellular effects.
Conclusions:
- The IGF system, particularly IGF-1, is a significant factor in atherosclerosis progression.
- PAPP-A critically modulates IGF-1's actions within the atherosclerotic environment.
- Understanding these interactions offers potential therapeutic targets for atherosclerosis.
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