ArticlePhysiological reports2019
Klf4, Klf2, and Zfp148 activate autophagy-related genes in smooth muscle cells during aortic aneurysm formation.
Article in Physiological reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 33 citations in OpenAlex.
- Sirtuin 1 Activation Mitigates Murine Vasculitis Severity by Promoting Mitophagy.Circulation research · 2026Article
- KLF4 overexpression in CAR T cells enhances antitumor potency by preventing exhaustion.Journal for immunotherapy of cancer · 2026Article
- Sirtuin 1 Activation Mitigates Murine Vasculitis Severity by Promoting Autophagy and Mitophagy.bioRxiv : the preprint server for biology · 2025Article
- Transcriptional regulation of autophagy in skeletal muscle stem cells.Disease models & mechanisms · 2025Review
- FAM3A reshapes VSMC fate specification in abdominal aortic aneurysm by regulating KLF4 ubiquitination.Nature communications · 2023Article
- Targeted PERK inhibition with biomimetic nanoclusters confers preventative and interventional benefits to elastase-induced abdominal aortic aneurysms.Bioactive materials · 2023Article
- Transcriptional regulation of autophagy and its implications in human disease.Cell death and differentiation · 2023Review
- CCN2 deficiency in smooth muscle cells triggers cell reprogramming and aggravates aneurysm development.JCI insight · 2023Article
- Kruppel-like factor 2 contributes to blood-spinal cord barrier integrity and functional recovery from spinal cord injury by augmenting autophagic flux.Theranostics · 2023Article
- KLF2 alleviates endothelial cell injury and inhibits the formation of THP‑1 macrophage‑derived foam cells by activating Nrf2 and enhancing autophagy.Experimental and therapeutic medicine · 2022Article
- SDF-1α/CXCR4 Pathway Mediates Hemodynamics-Induced Formation of Intracranial Aneurysm by Modulating the Phenotypic Transformation of Vascular Smooth Muscle Cells.Translational stroke research · 2022Article
- Endothelial pannexin-1 channels modulate macrophage and smooth muscle cell activation in abdominal aortic aneurysm formation.Nature communications · 2022Article
- The Role of KLF2 in the Regulation of Atherosclerosis Development and Potential Use of KLF2-Targeted Therapy.Biomedicines · 2022Review
- Leveraging cell-type-specific regulatory networks to interpret genetic variants in abdominal aortic aneurysm.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mesenchymal Stem Cells Alter MicroRNA Expression and Attenuate Thoracic Aortic Aneurysm Formation.The Journal of surgical research · 2021Article
- Telocytes in the human ascending aorta: Characterization and exosome-related KLF-4/VEGF-A expression.Journal of cellular and molecular medicine · 2021Article
- Autophagy-mitophagy induction attenuates cardiovascular inflammation in a murine model of Kawasaki disease vasculitis.JCI insight · 2021Article
- Curcumin nicotinate suppresses abdominal aortic aneurysm pyroptosis via lncRNA PVT1/miR-26a/KLF4 axis through regulating the PI3K/AKT signaling pathway.Toxicology research · 2021Article
- Different types of cell death in vascular diseases.Molecular biology reports · 2021Review
- Single-cell RNA sequencing reveals the cellular heterogeneity of aneurysmal infrarenal abdominal aorta.Cardiovascular research · 2021Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Abdominal aortic aneurysms (AAAs) are a progressive dilation of the aorta that is characterized by an initial influx of inflammatory cells followed by a pro-inflammatory, migratory, proliferative, and eventually apoptotic smooth muscle cell phenotype. In recent years, the mechanisms related to the initial influx of inflammatory cells have become well-studied; the mechanisms related to chronic aneurysm formation, smooth muscle cell apoptosis and death are less well-characterized. Autophagy is a generally believed to be a protective cellular mechanism that functions to recycle defective proteins and cellular organelles to maintain cellular homeostasis. Our goal with the present study was to investigate the role of autophagy in smooth muscle cells during AAA formation. Levels of the autophagy factors, Beclin, and LC3 were elevated in human and mouse AAA tissue via both qPCR and immunohistochemical analysis. Confocal staining in human and mouse AAA tissue demonstrated Beclin and LC3 were present in smooth muscle cells during AAA formation. Treatment of smooth muscle cells with porcine pancreatic elastase or interleukin (IL)-1β activated autophagy-related genes in vitro while treatment with a siRNA to Kruppel-like transcription factor 4 (Klf4), Kruppel-like transcription factor 2 (Klf2) or Zinc-finger protein 148 (Zfp148) separately inhibited activation of autophagy genes. Chromatin immunoprecipitation assays demonstrated that Klf4, Klf2, and Zfp148 separately bind autophagy genes in smooth muscle cells following elastase treatment. These results demonstrate that autophagy is an important mechanism related to Klfs in smooth muscle cells during AAA formation.
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