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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.
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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