Author Correction Published: Macrophage protein aP2 Safeguards Against Atherosclerosis in Apolipoprotein E-Deficient Mice
boston, MA & Nashville, TN – A correction has been issued regarding research published previously detailing the role of macrophage fatty-acid-binding protein aP2 in atherosclerosis. The study, conducted by researchers at Harvard School of Public Health and Vanderbilt University Medical Center, clarifies that a lack of aP2 actually protects mice deficient in apolipoprotein E against the advancement of the disease.
The original investigation, involving a collaborative team led by Gökhan S. Hotamisligil of Harvard and Macree F. Linton of Vanderbilt, examined the impact of aP2 – a protein involved in intracellular lipid metabolism – on atherosclerosis progression in apolipoprotein E-deficient mice, a common model for the human disease. Researchers initially observed a seemingly paradoxical effect: aP2 deficiency appeared to mitigate atherosclerosis despite increased lipid accumulation in macrophages.
Further analysis revealed that the absence of aP2 alters macrophage metabolism, leading to reduced inflammatory responses and ultimately, protection against plaque formation.The team, including Liza Makowski, Kazuhisa Maeda, K. Teoman Uysal, B. Boord B.Babaev, Fazio Serge, Maureen A. Morgan, Rex A. Parker, Jill Suttles, and Sergio Fazio, steadfast that aP2 normally promotes pro-atherogenic pathways within macrophages.
“These findings highlight a previously unappreciated role for aP2 in macrophage function and its contribution to atherosclerosis pathogenesis,” explained Dr. Hotamisligil. “Targeting aP2 could represent a novel therapeutic strategy for preventing or treating this widespread cardiovascular disease.”
The correction underscores the importance of rigorous scientific investigation and the iterative nature of finding.Atherosclerosis, a leading cause of heart attack and stroke, remains a significant public health challenge, affecting millions worldwide. Understanding the intricate mechanisms driving its development is crucial for identifying new and effective interventions. This revised understanding of aP2’s role adds a critical piece to that puzzle.
