ArticlePhysiological reports2017
Intimal hyperplasia induced by vascular intervention causes lipoprotein retention and accelerated atherosclerosis.
Article in Physiological reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Application of Nanoliposome Alprostadil in the Perioperative Period of Percutaneous Coronary Intervention to Reduce In-Stent Restenosis: A Systematic Review and Meta-Analysis.Journal of interventional cardiology · 2023Pooled it
- ZHX2 Alleviates Vascular Remodeling and Smooth Muscle Cell Proliferation by Transcriptional Regulation of GADD45G.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Hypertensive Nephrosclerosis: Pathological Changes and Overlap with Diabetic Nephropathy.Cureus · 2025Review
- Apolipoprotein B-containing lipoproteins in atherogenesis.Nature reviews. Cardiology · 2025Review
- Implantable Biosensors for Vascular Diseases: Directions for the Next Generation of Active Diagnostic and Therapeutic Medical Device Technologies.Biosensors · 2025Review
- The incidence rate and histological characteristics of intimal hyperplasia in elastase-induced experimental abdominal aortic aneurysms in mice.Animal models and experimental medicine · 2024Article
- Hypertensive Pressure Mechanosensing Alone Triggers Lipid Droplet Accumulation and Transdifferentiation of Vascular Smooth Muscle Cells to Foam Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- iPLA2 inhibition blocks LysoPC-induced TRPC6 externalization and promotes Re-endothelialization of carotid injuries in hypercholesterolemic mice.Cell calcium · 2023Article
- Role of PDE10A in vascular smooth muscle cell hyperplasia and pathological vascular remodelling.Cardiovascular research · 2022Article
- Review of Polymeric Biomimetic Small-Diameter Vascular Grafts to Tackle Intimal Hyperplasia.ACS omega · 2022Review
- Interleukin 6-regulated macrophage polarization controls atherosclerosis-associated vascular intimal hyperplasia.Frontiers in immunology · 2022Article
- Article
- Antibodies against apoB100 peptide 210 inhibit atherosclerosis in apoEScientific reports · 2021Article
- Review
- Effects of Kindlin-2 on proliferation and migration of VSMC and integrinβ1 andβ3 activity via FAK-PI3K signaling pathway.PloS one · 2020Article
- A role for proteoglycans in vascular disease.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- ApoB-100 Lipoprotein Complex Formation with Intima Proteoglycans as a Cause of Atherosclerosis and Its Possible Ex Vivo Evaluation as a Disease Biomarker.Journal of cardiovascular development and disease · 2018Review
- Hypoxia/reperfusion predisposes to atherosclerosis.PloS one · 2018Article
- Intimal hyperplasia induced by vascular intervention causes lipoprotein retention and accelerated atherosclerosis.Physiological reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accelerated atherosclerosis diminishes the long term patency of vascular interventions, such as percutaneous coronary intervention and implantation of saphenous vein grafts. However, the cause of this accelerated atherosclerosis is unclear. In this study, we tested the hypothesis that intimal hyperplasia formed following vascular intervention promotes retention of atherogenic lipoproteins. Intimal hyperplasia was surgically induced in the mouse common carotid artery. The surgery was combined with different mouse models of hypercholesterolemia to obtain different cholesterol levels and to control the onsets of hypercholesterolemia. Three weeks after surgery, samples were immunostained for apoB lipoproteins, smooth muscle cells and leukocytes. Already at mild hypercholesterolemia (193 mg/dL), pronounced apoB lipoprotein retention was found in the extracellular matrix in both intimal hyperplasia and the injured underlying media. In contrast, minimal retention was detected in the uninjured proximal region of the same vessel, or in vessels from mice with normal cholesterol levels (81 mg/dL). Induction of aggravated hypercholesterolemia 3 weeks after surgery, when a mature intimal hyperplasia had been formed, caused a very rapid development of atherosclerotic lesions. Mechanistically, we show that lipoprotein retention was almost exclusively dependent on electrostatic interactions to proteoglycan glycosaminoglycans, and the lipoprotein retention to intimal hyperplasia could be inhibited in vivo using glycosaminoglycan-binding antibodies. Thus, formation of intimal hyperplasia following vascular intervention makes the vessel wall highly susceptible for lipoprotein retention and accelerated atherosclerosis. The increased lipoprotein retention in intimal hyperplasia can be targeted by blocking the interaction between apoB lipoproteins and glycosaminoglycans in the extracellular matrix.
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Registered trials
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.