Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2025;32(17):3423-3437.
doi: 10.2174/0109298673279032231214110313.

Multifaceted Nature of HuR in Atherosclerosis Development

Affiliations
Review

Multifaceted Nature of HuR in Atherosclerosis Development

Yan-Xia Wang et al. Curr Med Chem. 2025.

Abstract

HuR (Human antigen R) is an RNA binding protein (RBP) that specifically binds to certain RNA sequences, influencing post-transcriptional regulation. HuR is primarily involved in tumor regulation, as well as cell growth, proliferation, inflammation, and angiogenesis. HuR is implicated in endothelial activation, smooth muscle proliferation, inflammatory response, macrophage apoptosis, lipid regulation, and autophagy, playing a crucial regulatory role in atherosclerosis. Accumulating evidence suggests that HuR has dual roles in AS. On the one hand, HuR expedites the development of AS by facilitating endothelial activation, smooth muscle proliferation, and inflammation. On the contrary, it exerts beneficial effects by reducing macrophage apoptosis, regulating lipid efflux, and increasing autophagy. In this review, we aim to provide a comprehensive summary of the role of HuR in the development of AS by examining its involvement in cellular mechanisms, inflammation, autophagy, and apoptosis. Additionally, we discuss the mechanisms of drugs that target HuR, with the goal of offering new perspectives for the treatment of AS.

Keywords: 3‘ UTR; Atherosclerosis; embryonic lethal.; endothelial cells; human antigen R; nucleoplasmic translocation.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Stellos K.; Gatsiou A.; Stamatelopoulos K.; Perisic Matic L.; John D.; Lunella F.F.; Jaé N.; Rossbach O.; Amrhein C.; Sigala F.; Boon R.A.; Fürtig B.; Manavski Y.; You X.; Uchida S.; Keller T.; Boeckel J.N.; Franco-Cereceda A.; Maegdefessel L.; Chen W.; Schwalbe H.; Bindereif A.; Eriksson P.; Hedin U.; Zeiher A.M.; Dimmeler S.; Adenosine-to-inosine RNA editing controls cathepsin S expression in atherosclerosis by enabling HuR-mediated post-transcriptional regulation. Nat Med 2016,22(10),1140-1150 - DOI - PubMed
    1. Bravo-San Pedro J.M.; Kroemer G.; Galluzzi L.; Autophagy and mitophagy in cardiovascular disease. Circ Res 2017,120(11),1812-1824 - DOI - PubMed
    1. Tapeinos C.; Gao H.; Bauleth-Ramos T.; Santos H.A.; Progress in stimuli-responsive biomaterials for treating cardiovascular and cerebrovascular diseases. Small 2022,18(36),2200291 - DOI - PubMed
    1. Grammatikakis I.; Abdelmohsen K.; Gorospe M.; Posttranslational control of function. Wiley Interdiscip Rev RNA 2017,8(1),e1372 - DOI - PubMed
    1. Vo D.T.; Abdelmohsen K.; Martindale J.L.; Qiao M.; Tominaga K.; Burton T.L.; Gelfond J.A.L.; Brenner A.J.; Patel V.; Trageser D.; Scheffler B.; Gorospe M.; Penalva L.O.F.; The oncogenic RNA-binding protein Musashi1 is regulated by HuR via mRNA translation and stability in glioblastoma cells. Mol Cancer Res 2012,10(1),143-155 - DOI - PubMed