ReviewFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025
From Bench to Clinic: Advances in Anti-Inflammatory Therapies for Atherosclerotic Coronary Artery Disease.
Review in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Cluster of Differentiation 36-Mediated Inflammation and Lipid Metabolism in Cardiovascular Diseases: From Mechanisms to Novel Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- The Role of Long Non-Coding RNA in Atherosclerosis: Mechanism and Intervention of Traditional Chinese Medicine.International journal of molecular sciences · 2026Review
- Pathological mechanisms and research progress of multilevel intervention therapy for coronary heart disease.Frontiers in immunology · 2026Review
- Persistent residual inflammatory risk at 1 month after contemporary PCI: rationale for routine hsCRP reassessment and dual-target therapy.Frontiers in immunology · 2026Review
- GLP-1 receptor agonists alleviate inflammatory responses and endothelial dysfunction in atherosclerosis by activating the Sema3A/NRP1 pathway.Frontiers in cardiovascular medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Atherosclerosis (AS) is a chronic, progressive inflammatory disorder characterized by the deposition of lipid-laden plaques, infiltration of immune cells, and remodeling of vascular structures within arterial walls. It remains the primary pathological driver of atherosclerotic coronary artery disease (ASCAD) and a major contributor to global mortality. While conventional lipid-lowering therapies, particularly statins, have significantly reduced the incidence of ASCAD by targeting hyperlipidemia, a considerable residual inflammatory risk continues to exist. This unresolved inflammation exacerbates plaque vulnerability, increases the likelihood of rupture, and precipitates thrombotic complications. Recent breakthroughs in understanding the complex inflammatory mechanisms underlying AS, including endothelial dysfunction, macrophage polarization, T-cell activation, and the release of pro-inflammatory cytokines, have revealed novel therapeutic targets. This mechanistic insight has spurred the development of innovative anti-inflammatory strategies, including monoclonal antibodies targeting specific cytokines (e.g., IL-1β, TNF-α), epigenetic modulators, and immune-based interventions. This review synthesizes the current understanding of the inflammatory pathogenesis of AS, evaluates the translational potential of emerging anti-inflammatory therapies, and discusses the challenges in optimizing the balance between efficacy and safety. By bridging discoveries in basic science with clinical applicability, this analysis aims to guide future research and foster therapeutic innovations in combating ASCAD.
Indexed as
Identifiers
What Socratic 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 Socratic graph.