ArticleCell death and differentiation2025
CKLF1 disrupts microglial efferocytosis following acute ischemic stroke by binding to phosphatidylserine.
Article in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Neuronal Apoptotic Bodies Facilitate Japanese Encephalitis Virus Infection and Pathogenicity.Journal of extracellular vesicles · 2026Article
- Ginsenoside Rg1 alleviates post-ischemic stroke neuroinflammation by inhibiting CKLF1-mediated suppression of dead/dying neuron clearance.Acta pharmaceutica Sinica. B · 2026Article
- A neutrophil-intrinsic CKLF1-PKM2 axis drives glycolytic flux for de novo DAG synthesis and pro-inflammatory ROS production.Cell death and differentiation · 2026Article
- Efferocytosis: unifying pathogenic hub in metabolic disorders-mechanistic landscapes, targeted therapies and translational bottlenecks.Frontiers in immunology · 2026Review
- Efferocytosis in Health and Disease.MedComm · 2025Review
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Authors and funding
14 authors.
Funding
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Abstract
Efferocytosis is crucial for the clearance of apoptotic cells (ACs) following acute ischemic stroke (AIS), however, its mechanism remains unclear. This study reveals that chemokine-like factor 1 (CKLF1) disrupts efferocytosis by promoting AC finding and internalization while impairing AC degradation in microglia. CKLF1 deficiency reduced the proportion of ACs and lowered levels of damage-associated molecular patterns. Mechanistically, CKLF1 binds to phosphatidylserine on apoptotic neurons/blebs, recruiting microglia to the ischemic penumbra via a C-C chemokine receptor 4 (CCR4)-dependent pathway. Apoptotic blebs with CKLF1 are engulfed into microglia, triggering the rapid production of interleukin-6 (IL6). IL6 enhances AC internalization through the signal transducer and activator of transcription 3 (STAT3)-vav guanine nucleotide exchange factor 1 (VAV1)-ras-related C3 botulinum toxin substrate 1 (RAC1) signaling cascade but simultaneously inhibits transcription factor EB (TFEB) nuclear translocation, leading to lysosomal dysfunction. This effect results in AC accumulation, compromising microglial efferocytosis efficiency and integrity. These findings uncover a novel regulatory axis induced by CKLF1, emphasizing the complex balance between AC internalization and degradation in microglial efferocytosis.
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