ArticleHypertension (Dallas, Tex. : 1979)2009
Glutathione S-transferase-micro1 regulates vascular smooth muscle cell proliferation, migration, and oxidative stress.
Article in Hypertension (Dallas, Tex. : 1979), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.
- Association between the null polymorphisms of GSTT1 and GSTM1 and the risk of gestational diabetes mellitus: a systematic review and meta-analysis.BMC endocrine disorders · 2025Pooled it
- Trans-ethnic Fine Mapping Highlights Kidney-Function Genes Linked to Salt Sensitivity.American journal of human genetics · 2016Pooled it
- An in-depth analysis of the molecular changes induced by short-term calorie restriction before living kidney donation.npj aging · 2026Article
- Integrated Single-Cell Multi-Omics Analysis Reveals That a CD8International journal of molecular sciences · 2026Article
- Integrative Transcriptomic and Proteomic Analysis RevealsAnimals : an open access journal from MDPI · 2025Article
- Toxicological Response of the BEAS-2B Cell After Acute Exposure at the Air-Liquid Interface to Ethylbenzene and m-Xylene Alone and in Binary Mixtures.Journal of applied toxicology : JAT · 2025Article
- Endothelial defects unveil cardiovascular phenotype in iPSC-based disease modelling across three generations of a DiGeorge syndrome family.Research square · 2025Article
- Mathurameha ameliorates cardiovascular complications in high-fat diet/low-dose streptozotocin-induced type 2 diabetic rats: insights from histological and proteomic analysis.Journal of molecular histology · 2024Article
- The micro-743a-3p-GSTM1 pathway is an endogenous protective mechanism against alcohol-related liver disease in mice.Cellular & molecular biology letters · 2024Article
- Buspirone Enhances Cell Survival and Preserves Structural Integrity during Oxidative Injury to the Retinal Pigment Epithelium.Antioxidants (Basel, Switzerland) · 2023Article
- Mechanisms of Small Intestine Involvement in Obesity-Induced Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Association of GSTM1 Deletion With Progression of CKD in Children: Findings From the Chronic Kidney Disease in Children (CKiD) Study.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2022Observational
- The interaction mechanism of nickel ions with L929 cells based on integrative analysis of proteomics and metabolomics data.Regenerative biomaterials · 2022Article
- Review
- GSTM1 Modulates Expression of Endothelial Adhesion Molecules in Uremic Milieu.Oxidative medicine and cellular longevity · 2021Article
- Article
- Exercise-Induced Regulation of Redox Status in Cardiovascular Diseases: The Role of Exercise Training and Detraining.Antioxidants (Basel, Switzerland) · 2019Review
- Article
- The Loss ofJournal of the American Society of Nephrology : JASN · 2017Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Glutathione S-transferase-micro1, GSTM1, belongs to a superfamily of glutathione S-transferases that metabolizes a broad range of reactive oxygen species and xenobiotics. Across species, genetic variants that result in decreased expression of the Gstm1 gene are associated with increased susceptibility for vascular diseases, including atherosclerosis in humans. We previously identified Gstm1 as a positional candidate in our gene mapping study for susceptibility to renal vascular injury characterized by medial hypertrophy and hyperplasia of the renal vessels. To determine the role of Gstm1 in vascular smooth muscle cells (VSMCs), we isolated VSMCs from mouse aortas. We demonstrate that VSMCs from the susceptible C57BL/6 mice have reduced expression of Gstm1 mRNA and its protein product compared with that of the resistant 129 mice. After serum stimulation, C57BL/6 VSMCs proliferate and migrate at a much faster rate than 129 VSMCs. Furthermore, C57BL/6 VSMCs have higher levels of reactive oxygen species and exhibit exaggerated p38 mitogen-activated protein kinase phosphorylation after exposure to H(2)O(2). To establish causality, we show that knockdown of Gstm1 by small interfering RNA results in increased proliferation of VSMCs in a dose-dependent manner, as well as in increased reactive oxygen species levels and VSMC migration. Moreover, Gstm1 small interfering RNA causes increased p38 mitogen-activated protein kinase phosphorylation and attenuates the antiproliferative effect of Tempol. Our data suggest that Gstm1 is a novel regulator of VSMC proliferation and migration through its role in handling reactive oxygen species. Genetic variants that cause a decremental change in expression of Gstm1 may permit an environment of exaggerated oxidative stress, leading to susceptibility to vascular remodeling and 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.