ReviewClinical reviews in allergy & immunology2024
Cellular and Molecular Mechanisms of Mast Cells in Atherosclerotic Plaque Progression and Destabilization.
Review in Clinical reviews in allergy & immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Neuroimmune Regulation of Microvascular Inflammation: The Heart-Brain Axis, Mast Cells, and the Protective Role of Flavonoids-A Comprehensive Review.Biomedicines · 2026Review
- Research Progress on Marine Active Substances in Improving Atherosclerosis.Marine drugs · 2026Review
- B Cell Subsets and Atherosclerosis: Updates and Emerging Concepts.Immunological reviews · 2026Review
- Pathogenesis of plaque erosion.Trends in cardiovascular medicine · 2026Review
- The cardiovascular-immune axis: crosstalk and therapy in atherosclerosis, myocarditis and vasculitis.Frontiers in immunology · 2026Review
- Inflammatory immune mechanisms underlying the comorbidity of psoriasis and atherosclerosis: clinical implications.Frontiers in immunology · 2026Review
- Article
- Article
- Engineered immune-driven theranostics for clinical cardiology.Military Medical Research · 2025Review
- The Junction of Allergic Inflammation and Atherosclerosis: Pathways and Clinical Implications-A Review.Life (Basel, Switzerland) · 2025Review
- The Impact of Mast Cells on the Anatomy, Cellular Communication, and Molecular Immune Network of Lymph Nodes.Clinical reviews in allergy & immunology · 2025Review
- Immunomodulatory Significance of Mast Cell Exosomes (MC-EXOs) in Immune Response Coordination.Clinical reviews in allergy & immunology · 2025Review
- Extracellular vesicles: molecular messengers and new therapeutic targets in acute myocardial infarction.Frontiers in immunology · 2025Review
- The role of mitochondria-related genes and immune infiltration in carotid atherosclerosis: identification of hub targets through bioinformatics and machine learning approaches.Frontiers in genetics · 2025Article
- The "angiogenesis-plaque stability paradox" in atherosclerosis pathogenesis.Frontiers in cardiovascular medicine · 2025Review
- Cardiovascular manifestations in mast cell activation disease: key insights for cardiologists and angiologists.Frontiers in cardiovascular medicine · 2025Review
- Relationship Between Inflammatory Readings and the Degree of Coronary Atherosclerosis (Pilot Study).Journal of clinical medicine · 2024Article
- Relationships between systemic sclerosis and atherosclerosis: screening for mitochondria-related biomarkers.Frontiers in genetics · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 3 countries.
Funding
Abstract
Mast cells (MCs) are commonly recognized for their crucial involvement in the pathogenesis of allergic diseases, but over time, it has come to light that they also play a role in the pathophysiology of non-allergic disorders including atherosclerosis. The involvement of MCs in the pathology of atherosclerosis is supported by their accumulation in atherosclerotic plaques upon their progression and the association of intraplaque MC numbers with acute cardiovascular events. MCs that accumulate within the atherosclerotic plaque release a cocktail of mediators through which they contribute to neovascularization, plaque progression, instability, erosion, rupture, and thrombosis. At a molecular level, MC-released proteases, especially cathepsin G, degrade low-density lipoproteins (LDL) and mediate LDL fusion and binding of LDL to proteoglycans (PGs). Through a complicated network of chemokines including CXCL1, MCs promote the recruitment of among others CXCR2
Indexed as
Identifiers
What OpenQuestion holds
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.