ReviewCurrent atherosclerosis reports2025
Anti-Atherogenic Mechanisms and Therapies.
Review in Current atherosclerosis reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Butyrate and Butyrate-Producing Bacteria in Cardiovascular-Kidney-Metabolic Syndrome.Antioxidants (Basel, Switzerland) · 2026Review
- Transient Glycocalyx Remodeling by Intravenous Hyaluronidase in Atherosclerosis: A Hypothesis-Generating Review.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Fatty acid metabolism and lipid channeling in macrophages: mechanisms of inflammation, resolution, and lipotoxicity.Frontiers in immunology · 2026Review
- Metabolic Reprogramming and Cell Interaction in Atherosclerosis: From Molecular Mechanisms to Therapeutic Strategies.Journal of cardiovascular development and disease · 2025Review
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.
Funding
Abstract
purpose of reviewThis review examines anti-atherogenic mechanisms and the crucial role of efferocytosis in promoting inflammation resolution, with a focus on innovative, resolution-based therapeutic strategies that aim to restore vascular homeostasis and mitigate atherosclerosis progression. RECENT
findingsAtherosclerosis, a chronic inflammatory condition, is exacerbated by impaired efferocytosis, which contributes to plaque instability and the expansion of the necrotic core. Advanced molecular and cellular profiling has revealed diverse macrophage populations and their metabolic adaptations during efferocytosis, which drive the production of resolving mediators essential for tissue repair. Dysregulated signaling and metabolic pathways disrupt the efficient clearance of apoptotic cells, exacerbating inflammation. Molecular regulators, such as microRNAs, further impact efferocytosis, governing cardiovascular outcomes. Resolution-based therapies, including specialized pro-resolving mediators, peptides, and metabolites, enhance the successive clearance of apoptotic cells while maintaining host immune function, offering advantages over traditional immunosuppressive approaches. Additionally, vaccines targeting disease-specific antigens show promise in eliciting protective immune responses that can help ameliorate atherosclerosis. Efferocytosis is a key regulator of inflammation resolution in atherosclerosis, linking macrophage metabolism to plaque stability. Its disruption drives disease progression, but emerging therapies targeting resolution pathways, metabolic reprogramming, and immune modulation hold the potential for effective interventions. Advances in profiling technologies and targeted delivery systems will address translational challenges, paving the way for precision medicine in treating atherosclerotic cardiovascular disease.
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.