ArticleInternational journal of clinical and experimental pathology2018
Long non-coding RNA PlncRNA-1 regulates cell proliferation, apoptosis, and autophagy in septic acute kidney injury by regulating BCL2.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Epigenetic dysregulation of autophagy in sepsis-induced acute kidney injury: the underlying mechanisms for renoprotection.Frontiers in immunology · 2023Review
- LncRNA OIP5-AS1 reduces renal epithelial cell apoptosis in cisplatin-induced AKI by regulating the miR-144-5p/PKM2 axis.Biomedical journal · 2022Article
- An Update of Long-Noncoding RNAs in Acute Kidney Injury.Frontiers in physiology · 2022Review
- LncRNA PlncRNA-1 accelerates the progression of prostate cancer by regulating PTEN/Akt axis.Aging · 2021Article
- Long Noncoding RNA: Regulatory Mechanisms and Therapeutic Potential in Sepsis.Frontiers in cellular and infection microbiology · 2021Review
- Regulatory Role of Non-Coding RNAs on Immune Responses During Sepsis.Frontiers in immunology · 2021Review
- Hypomethylation of PlncRNA-1 promoter enhances bladder cancer progression through the miR-136-5p/Smad3 axis.Cell death & disease · 2020Article
- SIKIAT1/miR-96/FOXA1 axis regulates sepsis-induced kidney injury through induction of apoptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to elucidate the potential role of long non-coding RNA PlncRNA-1 in the septic acute kidney injury (AKI). The expression of PlncRNA-1 in the serum of patients with septic AKI patient was detected. We then established lipopolysaccharide (LPS)-induced septic AKI model in NRK-52E cells to investigate the effects of the overexpression of PlncRNA-1 on cell proliferation, apoptosis, and autophagy. In addition, the regulatory relationship between PlncRNA-1 and B-cell lymphoma 2 (BCL2) was explored to further elucidate the regulatory mechanism of PlncRNA-1 in septic AKI. PlncRNA-1 is downregulated in the serum of patients with septic AKI and in LPS-induced septic AKI cells. The overexpression of PlncRNA-1 considerably increases proliferation and inhibits apoptosis and autophagy of LPS-induced septic AKI cells. In addition, PlncRNA-1 can promote BCL2 expression, and the overexpression of BCL2 enhances proliferation and inhibits apoptosis and autophagy of LPS-induced septic AKI cells. Our findings reveal that the overexpression of PlncRNA-1 may promote cell proliferation and inhibit apoptosis and autophagy in septic AKI by regulating BCL2 expression. PlncRNA-1 may serve as a potential biomarker or target for the diagnosis and treatment of septic AKI.
Indexed as
Identifiers
31938114PMC6957948W3027300863What 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.