ArticleThe Journal of clinical investigation2023
DPP4 inhibition impairs senohemostasis to improve plaque stability in atherosclerotic mice.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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
32 citing papers in PubMed, 35 citations in OpenAlex.
- Targeting senescent cells with dipeptidyl peptidase 4-CAR-NK cells alleviates liver fibrosis and reverses metabolic dysfunction.Acta pharmaceutica Sinica. B · 2026Article
- Characterizing the SASP-Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types.Aging cell · 2026Article
- Inflammation in atherosclerosis: Drivers, mechanisms and therapies.Acta pharmaceutica Sinica. B · 2026Review
- Pharmacological targeting of the senescence-associated secretory phenotype in atherosclerosis: therapeutic potential of senolytics and senomorphics.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Molecular damage associated with ageing drives inflammation in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- A senescence-based machine learning model prognosticates and personalizes therapy in cervical cancer.Translational cancer research · 2026Article
- HIF-1α attenuates ferroptosis-associated dermal fibroblast senescence via modulation of NF-κB-DPP4 signaling.Journal of translational medicine · 2026Article
- CD8Nature reviews. Cardiology · 2026Review
- Impairment of Macrophage Functions by the Senescence-Associated Secretory Phenotype of Vascular Smooth Muscle Cells-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Artery tertiary lymphoid organs, neuro-immune interaction and their mediators in atherosclerosis.Basic research in cardiology · 2026Review
- Characterizing the SASP-Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types.bioRxiv : the preprint server for biology · 2026Article
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
- Dipeptidyl peptidase-4 inhibitors are associated with a lower risk of osteoarthritis in patients with type 2 diabetes.Therapeutic advances in musculoskeletal disease · 2026Article
- Cellular senescence and metabolic aging in type 2 diabetes: mechanistic insights and translational implications.Frontiers in endocrinology · 2026Review
- GSDME-dependent pyroptosis drives abdominal aortic aneurysm via promoting vascular senescence.Nature communications · 2025Article
- Single-cell and spatial transcriptomics map senescent vascular cells in arterial remodeling during atherosclerosis in mice.Nature aging · 2025Article
- Molecular Insights into the Potential Cardiometabolic Effects of GLP-1 Receptor Analogs and DPP-4 Inhibitors.International journal of molecular sciences · 2025Review
- ITGA1, the alpha 1 subunit of integrin receptor, is a novel marker of drug-resistant senescent melanoma cells in vitro.Archives of toxicology · 2025Article
- The role of mitochondrial dysfunction in the pathogenesis of atherosclerosis: A new exploration from bioinformatics analysis.Medicine · 2025Article
- Lactoferrin influences atherosclerotic progression by modulating macrophagic AMPK/mTOR signaling-dependent autophagy.Scientific reports · 2025Article
Corrections and comments
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Authors and funding
28 authors at 2 institutions in 2 countries.
Funding
Abstract
Senescent vascular smooth muscle cells (VSMCs) accumulate in the vasculature with age and tissue damage and secrete factors that promote atherosclerotic plaque vulnerability and disease. Here, we report increased levels and activity of dipeptidyl peptidase 4 (DPP4), a serine protease, in senescent VSMCs. Analysis of the conditioned media from senescent VSMCs revealed a unique senescence-associated secretory phenotype (SASP) signature comprising many complement and coagulation factors; silencing or inhibiting DPP4 reduced these factors and increased cell death. Serum samples from persons with high risk for cardiovascular disease contained high levels of DPP4-regulated complement and coagulation factors. Importantly, DPP4 inhibition reduced senescent cell burden and coagulation and improved plaque stability, while single-cell resolution of senescent VSMCs reflected the senomorphic and senolytic effects of DPP4 inhibition in murine atherosclerosis. We propose that DPP4-regulated factors could be exploited therapeutically to reduce senescent cell function, reverse senohemostasis, and improve vascular disease.
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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 Socratic graph.