ArticleNature communications2018
MT4-MMP deficiency increases patrolling monocyte recruitment to early lesions and accelerates atherosclerosis.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Pharmacological and Genetic Targeting of Inflammatory Chemokine Receptors CCR1, CCR2, and CCR5 in Atherosclerosis: A Systematic Review and Meta-Analysis of Preclinical Studies.Journal of the American Heart Association · 2026Pooled it
- Refractory pleural effusion in malignant hypertension leading to an unexpected diagnosis of tuberculosis: A case report.Experimental and therapeutic medicine · 2025Article
- Epigenetic drivers of metalloproteinases and metastasis.Trends in cell biology · 2025Review
- Matrix metalloproteinase-driven epithelial-mesenchymal transition: implications in health and disease.Journal of translational medicine · 2025Review
- Abnormal blood pressure among individuals evaluated for tuberculosis infection in a U.S. public health tuberculosis clinic.Epidemiology and infection · 2024Article
- Neutrophils insert elastase into hepatocytes to regulate calcium signaling in alcohol-associated hepatitis.The Journal of clinical investigation · 2024Article
- Molecular Mechanisms Driven by MT4-MMP in Cancer Progression.International journal of molecular sciences · 2023Review
- Identification of Potential Biomarkers for Coronary Artery Disease Based on Cuproptosis.Cardiovascular therapeutics · 2023Article
- Article
- Pro-Inflammatory Alterations of Circulating Monocytes in Latent Tuberculosis Infection.Open forum infectious diseases · 2022Article
- Article
- p38 MAPK priming boosts VSMC proliferation and arteriogenesis by promoting PGC1α-dependent mitochondrial dynamics.Scientific reports · 2022Article
- The immunomodulatory role of matrix metalloproteinases in colitis-associated cancer.Frontiers in immunology · 2022Review
- Smooth muscle-specific MMP17 (MT4-MMP) regulates the intestinal stem cell niche and regeneration after damage.Nature communications · 2021Article
- Metformin inhibits cholesterol‑induced adhesion molecule expression via activating the AMPK signaling pathway in vascular smooth muscle cells.Molecular medicine reports · 2021Article
- Intravascular Crawling of Patrolling Monocytes: A Lèvy-Like Motility for Unique Search Functions?Frontiers in immunology · 2021Review
- Soluble RARRES1 induces podocyte apoptosis to promote glomerular disease progression.The Journal of clinical investigation · 2020Article
- Role of MafB in macrophages.Experimental animals · 2020Review
- Chemokine Receptor 5, a Double-Edged Sword in Metabolic Syndrome and Cardiovascular Disease.Frontiers in pharmacology · 2020Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Matrix metalloproteinases are involved in vascular remodeling. Little is known about their immune regulatory role in atherosclerosis. Here we show that mice deficient for MT4-MMP have increased adherence of macrophages to inflamed peritonea, and larger lipid deposits and macrophage burden in atherosclerotic plaques. We also demonstrate that MT4-MMP deficiency results in higher numbers of patrolling monocytes crawling and adhered to inflamed endothelia, and the accumulation of Mafb+ apoptosis inhibitor of macrophage (AIM)+ macrophages at incipient atherosclerotic lesions in mice. Functionally, MT4-MMP-null Mafb+AIM+ peritoneal macrophages express higher AIM and scavenger receptor CD36, are more resistant to apoptosis, and bind acLDL avidly, all of which contribute to atherosclerosis. CCR5 inhibition alleviates these effects by hindering the enhanced recruitment of MT4-MMP-null patrolling monocytes to early atherosclerotic lesions, thus blocking Mafb+AIM+ macrophage accumulation and atherosclerosis acceleration. Our results suggest that MT4-MMP targeting may constitute a novel strategy to boost patrolling monocyte activity in early inflammation.
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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.