ReviewJournal of inflammation research2025
Atherosclerosis and Inflammation: Are the Rules of the Game Changing with Biological Therapies?
Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Mouse Models of Atherosclerosis: What They Teach Us, What They Miss, and When to Use Them.Bioengineering (Basel, Switzerland) · 2026Review
- Macrophage microRNAs integrating lipid metabolism and inflammation: Implications for atherosclerosis.Metabolism open · 2026Review
- Galectin-3 and Coronary Artery Disease: An Inflammation-Based Approach.Journal of clinical medicine · 2026Article
- Triggering receptor expressed on myeloid cell family in atherosclerosis: from mechanisms to intervention strategies.Cell communication and signaling : CCS · 2026Review
- Ultrasound-driven atherosclerosis nanomedicine: from mechanical, cavitation, and sonodynamic therapies to bedside translation.Journal of nanobiotechnology · 2025Review
- Inflammation, Autonomic Control, and Adiposity in Adolescents: Links to Early Cardiovascular Risk.Life (Basel, Switzerland) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Atherosclerosis is a chronic, progressive vascular disease characterized not only by lipid accumulation but also by sustained inflammation. Recent evidence has highlighted the critical role of immune pathways and pro-inflammatory cytokines in plaque formation, progression, and destabilization. Aim: This narrative review aims to summarize current knowledge regarding the role of inflammation in atherosclerosis and evaluate the therapeutic potential of biologic agents targeting specific inflammatory pathways. Methods: A comprehensive literature search was conducted using keywords such as "atherosclerosis", "inflammation", "biologic agents", and "cytokine inhibitors". Recent clinical trials and relevant experimental studies were analyzed and synthesized narratively. Results: Biologic agents targeting IL-1β, IL-6, IL-17A, and CD20+ B cells have shown promising results in reducing inflammation and improving cardiovascular outcomes in high-risk patients. Agents such as canakinumab, anakinra, tocilizumab, rituximab, secukinumab, and alirocumab demonstrate varying degrees of efficacy depending on the targeted pathway. However, concerns remain regarding immunosuppression, lipid alterations, cost, and long-term safety. Conclusion: Biologic agents offer a novel, mechanism-based therapeutic approach in managing atherosclerosis. While current data support their benefit in select patient groups, further research is needed to clarify long-term outcomes, safety, and real-world applicability. Personalized treatment strategies based on inflammatory profiles may enhance clinical benefit.
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Identifiers
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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.