ArticleActa pharmacologica Sinica2023
Bioinspired PROTAC-induced macrophage fate determination alleviates atherosclerosis.
Article in Acta pharmacologica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- TRIM24 stabilizes the p110 CUX1 oncoprotein via USP10 to promote chemoresistance in acute myeloid leukemia.Journal of translational medicine · 2026Article
- Review
- Emerging Role and Potential Therapeutic Application of TRIM Proteins in Cardiovascular Diseases.Biomolecules · 2026Review
- The application of drug delivery systems based on targeted protein degradation chimeras in disease treatment strategies.Journal of nanobiotechnology · 2026Review
- Revolutionizing protein degradation: Harnessing nanoparticles for PROTAC delivery.Materials today. Bio · 2026Review
- Ceramide as a key regulatory factor in the impact of dietary inflammatory index on plaque stability.Scientific reports · 2026Article
- Biomaterials Promote the Regression of Atherosclerotic Plaque by Regulating Cell Behavior.International journal of nanomedicine · 2026Review
- Targeted protein degradation: species, diseases and efficient utilization.Journal of translational medicine · 2025Review
- Magnetically navigated nano-PROTAC ameliorates acute lung injury.Journal of nanobiotechnology · 2025Article
- Recent Advances in Nanomedicine: Cutting-Edge Research on Nano-PROTAC Delivery Systems for Cancer Therapy.Pharmaceutics · 2025Review
- Clinical diagnostic value of serum Trim24 in patients with atherosclerosis.Scientific reports · 2025Article
- PROTAC Technology as a New Tool for Modern Pharmacotherapy.Molecules (Basel, Switzerland) · 2025Review
- Ubiquitination-mediated protein homeostasis in cardiovascular diseases: molecular mechanisms and therapeutic opportunities.American journal of cardiovascular disease · 2025Review
- Nanotechnology Advances Proteolysis Targeting Chimeras (PROTACs): Transition From Basic Research to Clinical Application.International journal of nanomedicine · 2025Review
- The Magic and Mystery of TRIM65 in Diseases.Current medicinal chemistry · 2025Review
- Targeted protein degradation: advances in drug discovery and clinical practice.Signal transduction and targeted therapy · 2024Review
- Transcriptional co-activators: emerging roles in signaling pathways and potential therapeutic targets for diseases.Signal transduction and targeted therapy · 2023Review
- Cell Membrane-Camouflaged Nanoparticles Mediated Nucleic Acids Delivery.International journal of nanomedicine · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is a major cause of death and disability in cardiovascular disease. Atherosclerosis associated with lipid accumulation and chronic inflammation leads to plaques formation in arterial walls and luminal stenosis in carotid arteries. Current approaches such as surgery or treatment with statins encounter big challenges in curing atherosclerosis plaque. The infiltration of proinflammatory M1 macrophages plays an essential role in the occurrence and development of atherosclerosis plaque. A recent study shows that TRIM24, an E3 ubiquitin ligase of a Trim family protein, acts as a valve to inhibit the polarization of anti-inflammatory M2 macrophages, and elimination of TRIM24 opens an avenue to achieve the M2 polarization. Proteolysis-targeting chimera (PROTAC) technology has emerged as a novel tool for the selective degradation of targeting proteins. But the low bioavailability and cell specificity of PROTAC reagents hinder their applications in treating atherosclerosis plaque. In this study we constructed a type of bioinspired PROTAC by coating the PROTAC degrader (dTRIM24)-loaded PLGA nanoparticles with M2 macrophage membrane (MELT) for atherosclerosis treatment. MELT was characterized by morphology, size, and stability. MELT displayed enhanced specificity to M1 macrophages as well as acidic-responsive release of dTRIM24. After intravenous administration, MELT showed significantly improved accumulation in atherosclerotic plaque of high fat and high cholesterol diet-fed atherosclerotic (ApoE
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.