ReviewFrontiers in immunology2026
Pathological mechanisms and research progress of multilevel intervention therapy for coronary heart disease.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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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
2 citing papers in PubMed.
- Microbiota-innate immune crosstalk drives atherosclerosis: mechanisms, disease progression, and emerging therapeutic strategies.Frontiers in immunology · 2026Review
- Integrating Network Pharmacology and In Vitro Experiments to Elucidate the Antiatherosclerotic Mechanisms of Qingxin Tongmai Yin.Mediators of inflammation · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Coronary heart disease (CHD) is a chronic cardiovascular disease with coronary atherosclerosis as the main pathological basis. Its occurrence and progression are not a simple process of lipid deposition, but a systemic pathological process jointly driven by metabolic disorders, chronic low-grade inflammation, and immune imbalance. Recent studies have shown that endothelial dysfunction is a key event in the early occurrence of CHD. Abnormal lipid metabolism, immune cell infiltration, and continuous activation of inflammatory signals together promote plaque formation, maturation, and destabilization. Especially under the regulation of the metabolism-inflammation-immunity network, a positive feedback loop is formed between immune cell metabolic reprogramming, macrophage polarization, inflammasome activation, and oxidative stress response, which accelerates the progression of atherosclerosis and increases the risk of acute coronary events. Traditional therapeutic strategies centered on lipid-lowering, antiplatelet therapy, and revascularization can reduce the incidence of short-term events, but there are still limitations in long-term risk control and fundamental reversal of the disease. From a narrative perspective, this article summarizes the research progress of CHD in pathological mechanisms, metabolism and immune regulation, plaque instability, and risk factors from a systematic perspective and focuses on discussing the potential value of multilevel and systematic intervention strategies in the precise prevention and treatment of CHD, providing a theoretical basis for future translational research and personalized treatment.
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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.