ArticleMolecular medicine (Cambridge, Mass.)2023
HOXA1 participates in VSMC-to-macrophage-like cell transformation via regulation of NF-κB p65 and KLF4: a potential mechanism of atherosclerosis pathogenesis.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Tirzepatide mitigates atherosclerosis progression and modulates oxLDL-mediated proatherogenic effects in macrophages: evidence for M1/M2 homeostasis restoration.Archives of pharmacal research · 2026Article
- Lycium barbarum polysaccharide inhibits Hcy-induced vascular smooth muscle cells migration and invasion via upregulation of KLF4.Scientific reports · 2026Article
- A human blood-brain barrier model reveals pericytes as critical regulators of viral neuroinvasion.iScience · 2026Article
- VSMCs and the immune microenvironment: a multidimensional regulatory network driving vascular injury and repair.Frontiers in immunology · 2026Review
- Macrophage-like smooth muscle cells in atherosclerosis.Molecular biology reports · 2025Review
- Role of vascular smooth muscle phenotypic transformation induced by histone modifications in the development of abdominal aortic aneurysms.Clinical epigenetics · 2025Review
- MiR-7683-3p from M2-exosomes attenuated atherosclerosis by activating the PPARγ-LXRα-ABCG1 pathway mediated cholesterol efflux of vascular smooth muscle cell derived foam cells.Journal of nanobiotechnology · 2025Article
- Enhancer profiling uncovers Jmjd1c as an essential suppressor in neuropathic pain by targeting Socs3.Genes & diseases · 2025Article
- Long noncoding RNAs in familial hypercholesterolemia: biomarkers, therapeutics, and AI in precision medicine.Lipids in health and disease · 2025Review
- Protocatechuic Acid Attenuates Inflammation in Macrophage-like Vascular Smooth Muscle Cells in ApoENutrients · 2025Article
- TEAD1-Mediated Trans-Differentiation of Vascular Smooth Muscle Cells into Fibroblast-Like Cells Contributes to the Stabilization and Repair of Disrupted Atherosclerotic Plaques.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The role of protein S-acylation in vascular injury associated with metabolic disorders.Frontiers in endocrinology · 2025Review
- Quercetin Attenuates KLF4-Mediated Phenotypic Switch of VSMCs to Macrophage-like Cells in Atherosclerosis: A Critical Role for the JAK2/STAT3 Pathway.International journal of molecular sciences · 2024Article
- Oral Nanoformulations in Cardiovascular Medicine: Advances in Atherosclerosis Treatment.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Role of HOXA1-4 in the development of genetic and malignant diseases.Biomarker research · 2024Review
- An update on ox-LDL-inducing vascular smooth muscle cell-derived foam cells in atherosclerosis.Frontiers in cell and developmental biology · 2024Review
- Transcriptome sequencing and Mendelian randomization analysis identified biomarkers related to neutrophil extracellular traps in diabetic retinopathy.Frontiers in immunology · 2024Article
- Anemoside B4 attenuates abdominal aortic aneurysm by limiting smooth muscle cell transdifferentiation and its mediated inflammation.Frontiers in immunology · 2024Article
- Editorial: Transcriptional regulation in cardiovascular diseases.Frontiers in cardiovascular medicine · 2024Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMacrophage-like transformation of vascular smooth muscle cells (VSMCs) is a risk factor of atherosclerosis (AS) progression. Transcription factor homeobox A1 (HOXA1) plays functional roles in differentiation and development. This study aims to explore the role of HOXA1 in VSMC transformation, thereby providing evidence for the potential mechanism of AS pathogenesis.
methodsHigh fat diet (HFD)-fed apolipoprotein E knockout (ApoE
resultsIn the aortic root of AS mice, lipid deposition was severer and HOXA1 expression was higher than the wide-type mice fed with normal diet or HFD. Silencing of HOXA1 inhibited the AS-induced weight gain, inflammatory response, serum and liver lipid metabolism disorder and atherosclerotic plaque formation. Besides, lesions from AS mice with HOXA1 knockdown showed less trans-differentiation of VSMCs to macrophage-like cells, along with a suppression of krüppel-like factor 4 (KLF4) and nuclear factor (NF)-κB RelA (p65) expression. In vitro experiments consistently confirmed that HOXA1 knockdown suppressed lipid accumulation, VSMC-to-macrophage phenotypic switch and inflammation in POV-PC-treated VSMCs. Mechanism investigations further illustrated that HOXA1 transcriptionally activated RelA and KLF4 to participate in the pathological manifestations of VSMCs.
conclusionsHOXA1 participates in AS progression by regulating VSMCs plasticity via regulation of NF-κB p65 and KLF4. HOXA1 has the potential to be a biomarker or therapeutic target for AS.
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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.