ArticleBioengineered2022
Long non-coding RNA lincRNA-erythroid prosurvival (EPS) alleviates cerebral ischemia/reperfusion injury by maintaining high-temperature requirement protein A1 (Htra1) stability through recruiting heterogeneous nuclear ribonucleoprotein L (HNRNPL).
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- LincRNA-EPS alleviates osteoclastogenesis under inflammatory microenvironment through preventing excessive iron metabolism.Cell death & disease · 2026Article
- LincRNA-EPS inhibits caspase-11 and NLRP3 inflammasomes in gingival fibroblasts to alleviate periodontal inflammation.Cell proliferation · 2024Article
- The Role of LincRNA-EPS/Sirt1/Autophagy Pathway in the Neuroprotection Process by Hydrogen against OGD/R-Induced Hippocampal HT22 Cells Injury.Journal of personalized medicine · 2023Article
- LncRNA IL21-AS1 interacts with hnRNPU protein to promote IL21 overexpression and aberrant differentiation of Tfh cells in systemic lupus erythematosus.Clinical and translational medicine · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed at investigating the role and mechanism of lincRNA-EPS (erythroid prosurvival) in cerebral ischemia/reperfusion (CIR) injury. The results showed that the overexpression of lincRNA-EPS was able to reduce the levels of interleukin-6, tumor necrosis factor-alpha and interleukin-1β stimulated in the OGD-treated Neuro-2a (N-2a) cells. The levels of reactive oxygen species and malondialdehyde were enhanced while the superoxide dismutase levels were reduced by oxygen and glucose deprivation (OGD) treatment, in which the lincRNA-EPS overexpression could reverse this effect in the cells. LincRNA-EPS interacted with high-temperature requirement protein A1 (Htra1) and heterogeneous nuclear ribonucleoprotein L (HNRNPL), and their depletion inhibited the Htra1 mRNA stability in N-2a cells. HNRNPL knockdown blocked lincRNA-EPS overexpression-induced Htra1 expression in the cells. The depletion of Htra1 could rescue lincRNA-EPS overexpression-mediated N-2a cell injury, inflammation, and oxidative stress induced by OGD. Functionally, lincRNA-EPS alleviates CIR injury of the middle cerebral artery occlusion/reperfusion mice
Indexed as
Identifiers
What 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.