ReviewInternational journal of molecular sciences2025
Decoding the Kruppel-like Transcription Factors in Atherosclerosis: Insight from Molecular and Translational Perspectives.
Review in International journal of molecular sciences, 2025. 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
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
2 citing papers in PubMed.
- Regulatory roles and translational potential of the Kruppel-like factor family in liver disease.iLIVER · 2026Review
- The role of nitrogen dioxide in the prevalence of adverse cardiovascular and cerebrovascular diseases in China: a national multi-pollutant geospatial analysis.BMC public health · 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
6 authors.
Funding
Abstract
Atherosclerosis is a leading contributor to cerebrovascular and cardiovascular diseases, which can be driven by multiple pathological processes, including chronic inflammation, lipid dysregulation, and vascular remodeling. Currently, lifestyle intervention and pharmacological intervention, like statins, are recommended in clinical treatments. However, the mortality and morbidity rates caused by atherosclerosis remain high. Kruppel-like transcription factors (KLFs) are zinc-finger-containing transcription factors that are involved in various physiological and pathological processes. By modulating endothelial cell homeostasis, smooth muscle cell phenotypic switching, and inflammatory responses, members of the KLF family-particularly KLF2, KLF4, KLF5, KLF6, and KLF14-emerge as pivotal regulators in the initiation and progression of atherosclerotic lesions. In this review, we constructed a comprehensive network of KLFs in the pathogenesis of atherosclerosis. Based on the molecular mechanism, this review for the first time highlighted newly identified substances that exploit KLF-modulated pathways to attenuate atherosclerosis, and discussed emerging gene therapy and nanotechnology approaches, addressing both the therapeutic promise and challenges associated with targeted KLF modulation. This first offered new avenues for translational and precision medicine in atherosclerotic cardiovascular disease from the perspective of KLF.
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.