ArticleThe Journal of clinical investigation2026
Vascular smooth muscle cell-derived KIF13B inhibits proinflammatory responses to protect against atherosclerosis.
Article in The Journal of clinical investigation, 2026. 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
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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.
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.
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Who cites it
4 citing papers in PubMed.
- Adipocyte-Derived KIF13B Aggravates Obesity-Associated Metabolic Dysfunction via LRP1/PPARγ Signaling.MedComm · 2026Article
- Cell-Surface Signatures and Targets of Modulated Vascular Smooth Muscle Cells in Atherosclerosis: From State Identification to Precision Intervention.Journal of cardiovascular development and disease · 2026Review
- A Cathepsin-Triggered Size-Shrinkable Nanoparticle Enhances Fibrous Cap Penetration to Relieve Atherosclerosis.Advanced healthcare materials · 2026Article
- Re-analysis of single-cell transcriptomics reveals a critical role of TNS1 gene in driving contractile VSMC transdifferentiation into macrophage-like SMC and atherosclerotic plaque instability.Clinical and translational medicine · 2026Article
Corrections and comments
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Authors and funding
20 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerotic cardiovascular disease (ASCVD) remains a leading cause of death worldwide, with plaque instability being a major culprit. Phenotypic switching of vascular smooth muscle cells (VSMCs) is a central event in atherosclerosis, driving both plaque progression and stability, yet the underlying mechanisms are incompletely understood, limiting drug development targeting this process. Kinesin family member 13B (KIF13B) has been implicated in vascular biology, but its function in VSMCs is unknown. Here, we demonstrate that VSMC-specific deletion of Kif13b in mice overexpressing proprotein convertase subtilisin/kexin type 9 (PCSK9) exacerbates lesion development and impairs plaque stability, characterized by thinner fibrous caps and increased inflammation. Mechanistically, we determined that KIF13B facilitated the ubiquitination and proteasomal degradation of Krüppel-like factor 4 (KLF4) through the potassium channel tetramerization domain-containing 10-dependent (KCTD10-dependent) pathway. This KIF13B/KCTD10 axis reduced KLF4 protein levels, thereby inhibiting the proinflammatory responses and fibroblast-like transition of VSMCs to preserve their contractile phenotype. Importantly, the adverse effects of Kif13b deficiency on atherogenesis were effectively rescued by the small-molecule KLF4 inhibitor Kenpaullone. Our results unveil a VSMC-specific atheroprotective role for KIF13B, define the KIF13B/KCTD10/KLF4 pathway as a key regulatory axis governing VSMC fate and plaque stability, and validate the therapeutic potential of KIF13B for treating advanced atherosclerosis.
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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.