ArticlePloS one2014
Endotoxin induces fibrosis in vascular endothelial cells through a mechanism dependent on transient receptor protein melastatin 7 activity.
Article in PloS one, 2014. 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, 37 citations in OpenAlex.
- Enteral Nutrition in Critical Care: Pathogenesis, Complications, and the Therapeutic Promise of Mediterranean-Style Diets.Current gastroenterology reports · 2025Review
- Effect of Dietary Supplements with ω-3 Fatty Acids, Ascorbic Acid, and Polyphenolic Antioxidant Flavonoid on Gene Expression, Organ Failure, and Mortality in Endotoxemia-Induced Septic Rats.Antioxidants (Basel, Switzerland) · 2023Article
- Disseminated intravascular coagulation phenotype is regulated by the TRPM7 channel during sepsis.Biological research · 2023Article
- Potential of the TRPM7 channel as a novel therapeutic target for pulmonary arterial hypertension.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2022Review
- TRPM Channels in Human Diseases.Cells · 2020Review
- Factors Affecting the Formation and Treatment of Thrombosis by Natural and Synthetic Compounds.International journal of molecular sciences · 2020Review
- LPS promotes the progression of sepsis by activation of lncRNA HULC/miR-204-5p/TRPM7 network in HUVECs.Bioscience reports · 2020Article
- Ginsenoside Rg3 protects against iE-DAP-induced endothelial-to-mesenchymal transition by regulating the miR-139-5p-NF-κB axis.Journal of ginseng research · 2020Article
- TRPM7 mediates kidney injury, endothelial hyperpermeability and mortality during endotoxemia.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Endothelial Cells Exhibit Two Waves of P-selectin Surface Aggregation Under Endotoxic and Oxidative Conditions.The protein journal · 2019Article
- Endothelial to Mesenchymal Transition: Role in Physiology and in the Pathogenesis of Human Diseases.Physiological reviews · 2019Review
- TRPM4 regulates Akt/GSK3-β activity and enhances β-catenin signaling and cell proliferation in prostate cancer cells.Molecular oncology · 2018Article
- Endothelial fibrosis induced by suppressed STAT3 expression mediated by signaling involving the TGF-β1/ALK5/Smad pathway.Laboratory investigation; a journal of technical methods and pathology · 2017Article
- Human Peritoneal Mesothelial Cell Death Induced by High-Glucose Hypertonic Solution Involves CaFrontiers in physiology · 2017Article
- "TRP inflammation" relationship in cardiovascular system.Seminars in immunopathology · 2016Review
- TRPM4 Is a Novel Component of the Adhesome Required for Focal Adhesion Disassembly, Migration and Contractility.PloS one · 2015Article
- Oxidative stress mediates the conversion of endothelial cells into myofibroblasts via a TGF-β1 and TGF-β2-dependent pathway.Laboratory investigation; a journal of technical methods and pathology · 2014Article
- Endotoxin-induced endothelial fibrosis is dependent on expression of transforming growth factors β1 and β2.Infection and immunity · 2014Article
- Endothelial dysfunction in pulmonary arterial hypertension: an evolving landscape (2017 Grover Conference Series).Pulmonary circulationArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of systemic inflammatory diseases, including endotoxemia-derived sepsis syndrome, is characterized by endothelial dysfunction. It has been demonstrated that the endotoxin lipopolysaccharide (LPS) induces the conversion of endothelial cells (ECs) into activated fibroblasts through endothelial-to-mesenchymal transition mechanism. Fibrogenesis is highly dependent on intracellular Ca2+ concentration increases through the participation of calcium channels. However, the specific molecular identity of the calcium channel that mediates the Ca2+ influx during endotoxin-induced endothelial fibrosis is still unknown. Transient receptor potential melastatin 7 (TRPM7) is a calcium channel that is expressed in many cell types, including ECs. TRPM7 is involved in a number of crucial processes such as the conversion of fibroblasts into activated fibroblasts, or myofibroblasts, being responsible for the development of several characteristics of them. However, the role of the TRPM7 ion channel in endotoxin-induced endothelial fibrosis is unknown. Thus, our aim was to study whether the TRPM7 calcium channel participates in endotoxin-induced endothelial fibrosis. Using primary cultures of ECs, we demonstrated that TRPM7 is a crucial protein involved in endotoxin-induced endothelial fibrosis. Suppression of TRPM7 expression protected ECs from the fibrogenic process stimulated by endotoxin. Downregulation of TRPM7 prevented the endotoxin-induced endothelial markers decrease and fibrotic genes increase in ECs. In addition, TRPM7 downregulation abolished the endotoxin-induced increase in ECM proteins in ECs. Furthermore, we showed that intracellular Ca2+ levels were greatly increased upon LPS challenge in a mechanism dependent on TRPM7 expression. These results demonstrate that TRPM7 is a key protein involved in the mechanism underlying endotoxin-induced endothelial fibrosis.
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