Profilin 1 and Mitochondria-Partners in the Pathogenesis of Coronary Artery Disease?

Abstract

Atherosclerosis remains a large health and economic burden. Even though it has been studied for more than a century, its complex pathophysiology has not been elucidated. The relatively well-established contributors include: chronic inflammation in response to oxidized cholesterol, reactive oxygen species-induced damage and apoptosis. Recently, profilin 1, a regulator of actin dynamics emerged as a potential new player in the field. Profilin is abundant in stable atherosclerotic plaques and in thrombi extracted from infarct-related arteries in patients with acute myocardial infarction. The exact role of profilin in atherosclerosis and its complications, as well as its mechanisms of action, remain unknown. Here, we summarize several pathways in which profilin may act through mitochondria in a number of processes implicated in atherosclerosis.

• Authors: Elżbieta Paszek, Wojciech Zajdel, Tomasz Rajs, Krzysztof Żmudka, Jacek Legutko, Paweł Kleczyński
• Journal: International journal of molecular sciences (Int J Mol Sci) Vol. 22 Issue 3 (Jan 22 2021) ISSN: 1422-0067 [Electronic] Switzerland
• PMID: 33499277 (Publication Type: Journal Article, Review)

Chemical References

• Actins
• PFN1 protein, human
• Profilins
• Protein Isoforms
• Reactive Oxygen Species
• SIRT3 protein, human
• Sirtuin 3

Topics

• Actins (chemistry)
• Acute Disease
• Animals
• Apoptosis
• Atherosclerosis (metabolism)
• Coronary Artery Disease (metabolism)
• Humans
• Mice
• Mitochondria (metabolism)
• Myocardial Infarction (metabolism)
• Plaque, Atherosclerotic (pathology)
• Profilins (metabolism)
• Protein Isoforms
• Reactive Oxygen Species (metabolism)
• Reperfusion Injury (metabolism)
• Sirtuin 3 (metabolism)