ArticleScientific reports2017
Mir-21 Mediates the Inhibitory Effect of Ang (1-7) on AngII-induced NLRP3 Inflammasome Activation by Targeting Spry1 in lung fibroblasts.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- Angiotensin-(1-7) in asthma and pulmonary fibrosis: mechanisms of action, clinical safety, and nano-delivery strategies.Frontiers in pharmacology · 2026Review
- Erythropoietin alleviate obstructive renal fibrosis by regulating immunity and inflammation through miR-21-5p/SPRY1/ERK1/2/NF-κB pathway inhibition.Frontiers in molecular biosciences · 2026Article
- ACE2: Friend or Foe in Post-COVID-19 Neurodegeneration?International journal of molecular sciences · 2025Review
- 12/15-lipoxygenase orchestrates murine wound healing via PPARγ-activating oxylipins acting holistically to dampen inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Interplay between NETosis and the lncRNA-microRNA regulatory axis in the immunopathogenesis of cancer.Journal of physiology and biochemistry · 2025Review
- Review
- Effects of remote ischemic preconditioning and/or erythropoietin on lung injury induced by skeletal ischemia reperfusion: role of the NLRP3 inflammasome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025Article
- Oral Angiotensin-(1-7) formulation after established elastase-induced emphysema suppresses inflammation and restores lung architecture.Frontiers in pharmacology · 2025Article
- Mechanisms of Bleomycin-induced Lung Fibrosis: A Review of Therapeutic Targets and Approaches.Cell biochemistry and biophysics · 2024Review
- Mechanism of sodium butyrate, a metabolite of gut microbiota, regulating cardiac fibroblast transdifferentiation via the NLRP3/Caspase-1 pyroptosis pathway.Journal of cardiothoracic surgery · 2024Article
- Recombinant human angiotensin-converting enzyme 2 plays a protective role in mice with sepsis-induced cardiac dysfunction through multiple signaling pathways dependent on converting angiotensin II to angiotensin 1-7.Annals of translational medicine · 2023Article
- Angiotensin-converting enzyme - human amniotic mesenchymal stem cells improve pulmonary vascular remodeling in rats with pulmonary hypertension by promoting angiogenesis and counteracting inflammation.International journal of clinical and experimental pathology · 2023Article
- Alleviation of chemotherapy-induced acute lung injury via NLRP3/ ASC/ Caspase-1 signaling pathway.Toxicology research · 2022Article
- Pharmacological Blockade of NLRP3 Inflammasome/IL-1β-Positive Loop Mitigates Endothelial Cell Senescence and Dysfunction.Aging and disease · 2022Article
- Systems analysis shows that thermodynamic physiological and pharmacological fundamentals drive COVID-19 and response to treatment.Pharmacology research & perspectives · 2022Review
- RAAS, ACE2 and COVID-19; a mechanistic review.Saudi journal of biological sciences · 2021Review
- METTL3/N6-methyladenosine/ miR-21-5p promotes obstructive renal fibrosis by regulating inflammation through SPRY1/ERK/NF-κB pathway activation.Journal of cellular and molecular medicine · 2021Article
- Review
- The Impact of microRNAs in Renin-Angiotensin-System-Induced Cardiac Remodelling.International journal of molecular sciences · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA-21 (mir-21) induced by angiotensin II (AngII) plays a vital role in the development of pulmonary fibrosis, and the NLRP3 inflammasome is known to be involved in fibrogenesis. However, whether there is a link between mir-21 and the NLRP3 inflammasome in pulmonary fibrosis is unknown. Angiotensin-converting enzyme 2/angiotensin(1-7) [ACE2/Ang(1-7)] has been shown to attenuate AngII-induced pulmonary fibrosis, but it is not clear whether ACE2/Ang(1-7) protects against pulmonary fibrosis by inhibiting AngII-induced mir-21 expression. This study's aim was to investigate whether mir-21 activates the NLRP3 inflammasome and mediates the different effects of AngII and ACE2/Ang(1-7) on lung fibroblast apoptosis and collagen synthesis. In vivo, AngII exacerbated bleomycin (BLM)-induced lung fibrosis in rats, and elevated mir-21 and the NLRP3 inflammasome. In contrast, ACE2/Ang(1-7) attenuated BLM-induced lung fibrosis, and decreased mir-21 and the NLRP3 inflammasome. In vitro, AngII activated the NLRP3 inflammasome by up-regulating mir-21, and ACE2/Ang(1-7) inhibited NLRP3 inflammasome activation by down-regulating AngII-induced mir-21. Over-expression of mir-21 activated the NLRP3 inflammasome via the ERK/NF-κB pathway by targeting Spry1, resulting in apoptosis resistance and collagen synthesis in lung fibroblasts. These results indicate that mir-21 mediates the inhibitory effect of ACE2/Ang(1-7) on AngII-induced activation of the NLRP3 inflammasome by targeting Spry1 in lung fibroblasts.
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