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Access through your institution Buy or subscribe Atherosclerosis is an inflammatory degenerative disease of the arterial wall that can lead to cardiovascular accidents in later stages. This
complex disease shows accumulation of macrophages within the arterial neointima contributing to atherosclerotic plaque development. A study in _Nature Communications_ now shows the
importance of the transcription factor _Zeb1_ expressed in macrophages in atherosclerotic plaque formation and stability. When analyzing atherosclerosis-prone Apoe KO mice in which _Zeb1_
was ablated in myeloid cells, the researchers observed bigger plaques, larger lipid accumulation and systemic inflammation markers compared with the control Apoe KO group. Administration of
nanoparticles targeting macrophages to induce _Zeb1_ expression reduced the formation of atherosclerotic plaque in these mice. These results show that _Zeb1_ limits the accumulation of
lipids in macrophages and contributes to the stability of the atherosclerotic plaque. _Zeb1_, which prevents ruptures and cardiovascular accidents, could be a potential therapeutic target
for atherosclerosis. ORIGINAL REFERENCE: Martinez-Campanario, M.C. et al. _Nat. Commun_. 14, 8316 (2023) This is a preview of subscription content, access via your institution ACCESS OPTIONS
Access through your institution ADDITIONAL ACCESS OPTIONS: * Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support AUTHOR INFORMATION AUTHORS AND
AFFILIATIONS * Lab Animal http://www.nature.com/laban/ Jorge Ferreira Authors * Jorge Ferreira View author publications You can also search for this author inPubMed Google Scholar
CORRESPONDING AUTHOR Correspondence to Jorge Ferreira. RIGHTS AND PERMISSIONS Reprints and permissions ABOUT THIS ARTICLE CITE THIS ARTICLE Ferreira, J. ZEB1 role in atherosclerosis. _Lab
Anim_ 53, 27 (2024). https://doi.org/10.1038/s41684-024-01327-0 Download citation * Published: 02 February 2024 * Issue Date: February 2024 * DOI: https://doi.org/10.1038/s41684-024-01327-0
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