ArticleAmerican journal of translational research2021
Long non-coding RNA ANRIL mitigates neonatal hypoxic-ischemic brain damage via targeting the miR-378b/ATG3 axis.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Bridging development and disease: the potential of LncRNAs as biomarkers and therapeutics in pediatric neurological disorders.Pediatric research · 2026Review
- Xanthohumol ameliorates diabetic kidney disease through suppression of renal fibrosis by regulating SNHG10/miR-378b.Frontiers in pharmacology · 2025Article
- LncRNAs and CircRNAs as Strategies against Pathological Conditions Caused by a Hypoxic/Anoxic State.Biomolecules · 2023Review
- Roles of Non-Coding RNA in Alzheimer's Disease Pathophysiology.International journal of molecular sciences · 2023Review
- The Role of Pyroptosis and Autophagy in Ischemia Reperfusion Injury.Biomolecules · 2022Review
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
Hypoxic-ischemic brain injury (HIBD) is the most common form of brain injury in newborns and is a major burden on society. However, the molecular mechanism of HIBD remains unclear. Long non-coding RNA (lncRNA) has been demonstrated to be a key regulator in brain development and numerous neurological diseases. The present study identified the role and underlying mechanism of lncRNA antisense non-coding RNA in the INK4 locus (ANRIL) in HIBD. The data indicated that ANRIL expression was significantly increased in hypoxia-stressed primary neurons and PC12 cells. Silencing ANRIL aggravated oxygen-glucose deprivation-induced cell injury. Mechanistically, microRNA (miR)-378b was predicted and confirmed as a direct target of ANRIL. A miR-378b inhibitor counteracted the effect of ANRIL on hypoxia-induced cell injury. Furthermore, ANRIL positively regulated autophagy related 3 (ATG3) expression and promoted autophagy through competitively binding to miR-378b. Overall, the present findings suggest that ANRIL exerts its protective effects via binding to miR-378b and upregulating ATG3 expression, suggesting the potential of ANRIL as a protective target for HIBD.
Indexed as
Identifiers
34786084PMC8581876W3214118672What OpenQuestion holds
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.