Atherosclerosis
is a multifaceted disease characterised by chronic inflammation and
vascular remodelling, leading to plaque formation and cardiovascular
complications. Recent evidence highlights the critical role of epsins, a
family of endocytic proteins, in the pathogenesis of atherosclerosis.
This manuscript explores the multifarious functions of epsins in
atherosclerosis, focusing on their involvement in angiogenesis,
lymphangiogenesis, and the modulation of key signalling pathways. We
discuss how epsins facilitate EndoMT through their interaction with the
TGFβ signalling pathway, which contributes to vascular smooth muscle
cell-like phenotypes and plaque instability. Additionally, we examine
the therapeutic potential of targeting epsins, elucidating their
interactions with crucial partners such as LDLR, LRP-1, and TLR 2/4,
among others, in mediating lipid metabolism and inflammation.
Furthermore, we highlight the promising prospects of epsin-targeting
peptides and small interfering RNAs as therapeutic agents for
atherosclerosis treatment. Despite these advancements, the research
faces limitations, including a reliance on specific mouse models and a
need for comprehensive studies on the long-term effects of epsin
modulation. Therefore, future investigations should focus on elucidating
the detailed mechanisms of epsin function and their implications in
cardiovascular health, fostering collaborations to translate basic
research into innovative therapeutic strategies. This work underscores
the necessity for further exploration of epsins to unlock their full
therapeutic potential in combating atherosclerosis and related
cardiovascular diseases.
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