ArticleOxidative medicine and cellular longevity2022
NLRP3 Knockout Protects against Lung Injury Induced by Cerebral Ischemia-Reperfusion.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Immunomodulation for stroke-associated pneumonia: a systematic review of mechanistic insight and emerging therapeutic strategies in animal models.Frontiers in immunology · 2026Pooled it
- Barbaloin Alleviates Lung Ischemia-Reperfusion Injury by Dual-Targeting IL-6 and PNP.International journal of molecular sciences · 2026Article
- Esculin Alleviated NLRP3 Inflammasome Activation by Inducing PINK1/Parkin-Mediated Mitophagy in Cerebral Ischemia-Reperfusion Injury.Molecular neurobiology · 2026Article
- Protective mechanisms of exosomes derived from human umbilical cord mesenchymal stem cells in bronchopulmonary dysplasia.Physiological research · 2025Article
- MiR-100-5p-rich small extracellular vesicles from activated neuron to aggravate microglial activation and neuronal activity after stroke.Journal of nanobiotechnology · 2024Article
- ATG5 Knockdown Attenuates Ischemia‒Reperfusion Injury by Reducing Excessive Autophagy-Induced Ferroptosis.Translational stroke research · 2024Article
- METTL14 contributes to acute lung injury by stabilizing NLRP3 expression in an IGF2BP2-dependent manner.Cell death & disease · 2024Article
- Expression of NGF, proNGF, p75Clinics (Sao Paulo, Brazil) · 2024Article
- NLRP3 Inflammasome's Activation in Acute and Chronic Brain Diseases-An Update on Pathogenetic Mechanisms and Therapeutic Perspectives with Respect to Other Inflammasomes.Biomedicines · 2023Review
- Identification of cuproptosis-related biomarkers and analysis of immune infiltration in allograft lung ischemia-reperfusion injury.Frontiers in molecular biosciences · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methods: C57/BL6 wild-type (WT) and NLRP3-KO mice were used to construct middle cerebral artery occlusion (MCAO) models. 2,3,5-Triphenyltetrazolium chloride (TTC) was used to evaluate brain damage, and neurological deficits were assessed. Then, lung tissue injury was examined in the different groups of mice by hematoxylin-eosin (HE) staining. Inflammation (macrophage and neutrophil infiltration, NLRP3-associated inflammatory molecules) and oxidative stress (reactive oxygen species, ROS) in the lungs were comprehensively examined by immunofluorescence staining and Western blotting. Results: First, our findings demonstrated that NLRP3 knockout had a protective effect against cerebral ischemia-reperfusion injury after MCAO. Second, by reducing brain damage after MCAO, lung inflammation was also alleviated. Immunofluorescence staining showed that NLRP3-KO-MCAO mice had reduced inflammatory effector molecule (caspase-1 and IL-1 Conclusions: NLRP3 inflammasome knockout not only is beneficial for cerebral ischemia-reperfusion injury but also reduces the severity of poststroke lung injury by reducing brain damage. It has been confirmed that there is a relationship between central insult and peripheral organ injury, and protecting the brain can prevent peripheral organ damage.
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