ArticleJournal of molecular medicine (Berlin, Germany)2020
NLRP6 contributes to inflammation and brain injury following intracerebral haemorrhage by activating autophagy.
Article in Journal of molecular medicine (Berlin, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 31 citations in OpenAlex.
- Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026Article
- Article
- Association between the monocyte-to-lymphocyte ratio and 28-day all-cause mortality in sepsis-associated delirium patients: a retrospective study and machine learning.BMC infectious diseases · 2026Article
- Microglia‑mediated neuroinflammation in intracerebral hemorrhage: Pathological mechanisms and implications for therapeutic development (Review).International journal of molecular medicine · 2026Review
- Expression and analysis of NLRP6 in chronic gastritis in children.BMC gastroenterology · 2025Article
- Article
- Correlation between NLRP6 inflammasome and the levels of inflammatory cytokines IL-1b and IL-18 in serum of patients with Meniere's disease.Journal of medical biochemistry · 2025Article
- Inflammation in cancer: therapeutic opportunities from new insights.Molecular cancer · 2025Review
- Neuroprotective effect of Naochuxue prescription on intracerebral hemorrhage: inhibition of autophagy downregulating high mobility group box-1.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Article
- BRCC3 mediates inflammation and pyroptosis in cerebral ischemia/reperfusion injury by activating the NLRP6 inflammasome.CNS neuroscience & therapeutics · 2024Article
- Role of pyroptosis in the pathogenesis of various neurological diseases.Brain, behavior, and immunity · 2024Review
- The role of NLRP6 in the development and progression of neurological diseases.Molecular biology reports · 2024Review
- Review
- N6-methyladenosine demethylase FTO regulates synaptic and cognitive impairment by destabilizing PTEN mRNA in hypoxic-ischemic neonatal rats.Cell death & disease · 2023Article
- NPAS4 Exacerbates Pyroptosis via Transcriptionally Regulating NLRP6 in the Acute Phase of Intracerebral Hemorrhage in Mice.International journal of molecular sciences · 2023Article
- Spotlight on NLRP6 and Tumor Research Situation: A Potential Cancer Participant.Journal of immunology research · 2023Review
- The association between Monocyte-to-Lymphocyte ratio and postoperative delirium in ICU patients in cardiac surgery.Journal of clinical laboratory analysis · 2022Article
- Microglial pyroptosis: Therapeutic target in secondary brain injury following intracerebral hemorrhage.Frontiers in cellular neuroscience · 2022Review
- Autophagy regulates inflammation in intracerebral hemorrhage: Enemy or friend?Frontiers in cellular neuroscience · 2022Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is a crucial factor contributing to secondary brain injury after intracerebral haemorrhage (ICH). NLRP6, a member of nod-like receptors (NLRs) family, has been reported to participate in inflammation and host-defence in multiple diseases. Distinct from the other NLR family members, NLRP6 regulates inflammation in an inflammasome-dependent as well as an inflammasome-independent pathway. However, the role of NLRP6 in regulating signalling pathways during ICH is poorly understood. In the present study, we demonstrated that NLRP6 expression was upregulated after ICH, both in humans and in rats. Subsequently, we developed a rat model of ICH and found that NLRP6 knockdown reduced brain injury, alleviated inflammation, and suppressed autophagy following ICH. Further, results indicated that autophagy involved in NLRP6 mediated inflammation after ICH. Moreover, we found that NLRP6 mediated regulation of autophagy and inflammation was inflammasome-dependent. This study revealed the underlying molecular mechanism of NLRP6 in inflammation and highlights the therapeutic potential of targeting NLRP6 in secondary brain injury after ICH. KEY MESSAGES: • NLRP6 was upregulated following ICH in humans and rats. • NLRP6 knockdown reduced brain injury, alleviated inflammation, and suppressed autophagy following ICH. • NLRP6 aggravated inflammation after ICH by activating autophagy. • NLRP6 regulated inflammation and autophagy after ICH by activating inflammasome pathway.
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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.