Macrophage-derived KIF13B interacts with USP9X to attenuate abdominal aortic aneurysm development by potentiating TFEB stability.

{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:40963913", "kind": "science-record", "revision": 3, "content_hash": "sha256:556929eba8dbb5ab3eff3589540cbb05ba3b2216d1faf7bb89acbca02c6fd674", "created_at": "2026-11-01T20:31:03Z", "updated_at": "2026-11-01T22:14:43Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Macrophage-derived KIF13B interacts with USP9X to attenuate abdominal aortic aneurysm development by potentiating TFEB stability.", "doi": "10.7150/thno.118958", "pmid": "40963913", "authors": ["Jingxuan Chen", "Yitong Xu", "Huahui Yu", "Yiran Liu", "Guolin Miao", "Yufei Han", "Liwen Zheng", "Zeyu Cai", "Zihao Zhou", "Jinxuan Chen", "Sijing Shi", "Pingping Lai", "Wenxi Zhang", "Lianxin Zhang", "Si Mei", "Yinqi Zhao", "Ling Zhang", "Wei Huang", "Yuhui Wang", "Dongyu Zhao", "Wei Kong", "Yanwen Qin", "Erdan Dong", "Xunde Xian"], "journal": "Theranostics", "year": 2025, "abstract": "Rationale: Abdominal aortic aneurysm (AAA) is a highly lethal cardiovascular disorder for which there is no effective medication to date. Kinesin family member 13b (KIF13B), a vital motor protein, has been recently identified as a novel regulator of lipid metabolism. However, the role of KIF13B in AAA development has not been documented. Methods: We determined the expression of KIF13B in aortic tissues from clinical patients and porcine pancreatic elastase (PPE) or angiotensin II (ANG II)-induced AAA mouse models. To investigate the influence of KIF13B on AAA expansion, we established global, myeloid cell-specific and vascular smooth muscle cell (VSMC)-specific conditional Kif13b-deficient mice in PPE and/or ANG II-induced AAA models. Results: RNA-seq data from GEO database (GSE57691) revealed a significant decrease in KIF13B gene expression within the aortic tissues of patients with AAA. KIF13B protein levels were largely reduced in aortic tissue samples from patients and two mouse models with AAA. Complete inactivation of Kif13b or depleting Kif13b from myeloid cells but not smooth muscle cells (SMCs) exacerbated AAA development. Mechanistic studies identified transcription factor EB (TFEB) as a critical downstream target of KIF13B. KIF13B stabilized and upregulated TFEB by enhancing its deubiquitination through an interaction with deubiquitinase USP9X to maintain the proper function of lysosomes, thus inhibiting the senescence-associated secretory phenotype (SASP) and proinflammatory response of macrophages. Moreover, restoration of macrophage Kif13b or senolytic therapy dramatically mitigated AAA expansion in vivo. Conclusions: In the present study, we provided a new insight into the pathogenesis of AAA and defined a KIF13B-USP9X-TFEB axis that is essential for the regulation of macrophage function, suggesting that macrophage-derived Kif13b is a beneficial regulator of vascular homeostasis and targeting KIF13B could be a potential therapeutic approach for the treatment of human AAA disease in future clinical trial.", "claims": [{"id": "claim-method", "statement": "Furthermore, to explore the functional relevance of KIF13B in AAA, we performed gene set enrichment analysis (GSEA) using the AAA-associated transcriptome.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:40963913", "locator": "sections[7] \"KIF13B expression is decreased in aortic tissues of AAA patients and mouse models\" paragraph 2", "quote": "Furthermore, to explore the functional relevance of KIF13B in AAA, we performed gene set enrichment analysis (GSEA) using the AAA-associated transcriptome."}], "state": "complete"}, {"id": "claim-data-access", "statement": "The data supporting the findings of this study are available from the corresponding author upon reasonable request.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:40963913", "locator": "sections[20] \"Resource availability\" paragraph 2", "quote": "The data supporting the findings of this study are available from the corresponding author upon reasonable request."}], "state": "complete"}, {"id": "claim-target-result", "statement": "In the present study, we provided a new insight into the pathogenesis of AAA and defined a KIF13B-USP9X-TFEB axis that is essential for the regulation of macrophage function, suggesting that macrophage-derived Kif13b is a beneficial regulator of vascular homeostasis and targeting KIF13B could be a potential therapeutic approach for the treatment of human AAA disease in future clinical trial.", "kind": "qualitative", "target": null, "evidence": [{"asset": "source:pmid:40963913", "locator": "sections[0] \"Abstract\" paragraph 4", "quote": "In the present study, we provided a new insight into the pathogenesis of AAA and defined a KIF13B-USP9X-TFEB axis that is essential for the regulation of macrophage function, suggesting that macrophage-derived Kif13b is a beneficial regulator of vascular homeostasis and targeting KIF13B could be a potential therapeutic approach for the treatment of human AAA disease in future clinical trial."}], "state": "complete"}], "gaps": []}, "experiment": {"state": "partial", "objective": "In the present study, we provided a new insight into the pathogenesis of AAA and defined a KIF13B-USP9X-TFEB axis that is essential for the regulation of macrophage function, suggesting that macrophage-derived Kif13b is a beneficial regulator of vascular homeostasis and targeting KIF13B could be a potential therapeutic approach for the treatment of human AAA disease in future clinical trial.", "steps": [{"id": "read_published_estimate", "order": 1, "name": "Read the published estimate from the source", "kind": "other", "state": "complete", "blocked_on": null, "description": "The claim, method and evidence span published with the source article.", "duration_hours": null, "parameters": {}, "inputs": ["source:pmid:40963913"], "outputs": ["the published estimate and its evidence"], "instruments": [], "reagents": []}, {"id": "obtain_source_data", "order": 2, "name": "Obtain the source data from the named repository", "kind": "data-preparation", "state": "complete", "blocked_on": null, "description": "The GEO series accession resolves and its sample accessions are listed. 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Conclusions: In the present study, we provi", "(PPE) or angiotensin II (ANG II)-induced AAA mouse models. To investigate the influence of KIF1", "aortic tissue samples from patients and two mouse models with AAA. Complete inactivation of Ki", "if13b-/-) mice and floxed Kif13b (Kif13bf/f) mice were generated using CRISPR/Cas9 technology by th"], "order_basis": "paper_text_order:591", "id": "assay:1"}, {"role": "data_generation", "definition_id": "rna_seq", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.99, "evidence": ["E and/or ANG II-induced AAA models. Results: RNA-seq data from GEO database (GSE57691) revealed a", "ion between KIF13B and AAA, we analyzed bulk RNA-seq data from the GEO database (GSE57691), compr", "ent analysis (GSEA) using the AAA-associated transcriptome. KIF13B expression strongly correlated with"], "order_basis": "paper_text_order:839", "id": "assay:2"}, {"role": "data_generation", "definition_id": "transfection", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.85, "evidence": ["Kif13b (Kif13bf/f) mice were generated using CRISPR/Cas9 technology by the Institute of Laborato"], "order_basis": "paper_text_order:2491", "id": "assay:3"}, {"role": "data_generation", "definition_id": "ihc", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.99, "evidence": ["AA tissues compared to controls (Figure 1B). Immunofluorescence staining and Western blot analysis corrobora", "ative images of HE staining and co-localized immunofluorescence staining depict α-SMA (green), CD68 (grey),", "ive images of HE staining, EVG staining, and immunofluorescence staining depict α-SMA (green), CD68 (red), a", "ive images of HE staining, EVG staining, and immunofluorescence staining illustrate α-SMA (green), CD68 (red"], "order_basis": "paper_text_order:4954", "id": "assay:4"}, {"role": "data_generation", "definition_id": "western_blot", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.99, "evidence": ["(Figure 1B). Immunofluorescence staining and Western blot analysis corroborated these findings, showin", "cent normal aortas (ANAs) (n = 6/group). (D) Western blot analysis of KIF13B protein levels in human A", "of Kif13b mRNA expression (n = 3/group) and western blot analysis of KIF13B protein expression in WT"], "order_basis": "paper_text_order:4986", "id": "assay:5"}, {"role": "data_generation", "definition_id": "qpcr", "definition_version": "99e1195c7d6f", "definition_digest": null, "required_operations": [], "support_state": "partial", "source_hashes": {"assay_lexicon": "99e1195c7d6f"}, "confidence": 0.99, "evidence": ["orcine pancreatic elastase (PPE, n = 6). (G) qPCR analysis of Kif13b mRNA expression (n = 3/gr", "= 3) or angiotensin II (ANG II, n = 6). 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