ArticleInternational journal of clinical and experimental pathology2019
Transcription coactivator p300 promotes inflammation by enhancing p65 subunit activation in type 2 diabetes nephropathy.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 7 citations in OpenAlex.
- MiR-342-3p Attenuates Inflammation and Pyroptosis in Severe Community-Acquired Pneumonia by Targeting EP300.Biochemical genetics · 2026Article
- P300 in Inflammation: An Updated Perspective on Its Molecular Mechanisms and Therapeutic Potential.Inflammation · 2026Review
- Article
- Diabetes and Its Cardiovascular Complications: Potential Role of the Acetyltransferase p300.Cells · 2023Review
- Endothelial AMPKα1/PRKAA1 exacerbates inflammation in HFD-fed mice.British journal of pharmacology · 2022Article
- Inhibition of p300 by Garcinol Protects against Cisplatin-Induced Acute Kidney Injury through Suppression of Oxidative Stress, Inflammation, and Tubular Cell Death in Mice.Antioxidants (Basel, Switzerland) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundp300, a transcription co-activator, plays an important role in multicellular organisms and inflammation. However, the mechanism of p300 in type 2 diabetes nephropathy (T2DN) remains largely unknown. Our aim is to explore the mechanism of p300 in T2DN.
methodsA T2DN mice model was induced by db/db transgenic mice or a high fat diet for 24 weeks. The levels of IL-6 and TNF-α were examined by real-time PCR (RT-PCR) in the renal cortex and by an enzyme linked immunosorbent assay (ELISA) in the serum of the T2DN mice. p300 siRNA was used to knockdown the expression of p300, and His-tagged-p300 plasmid was used to overexpress the p300 protein level in podocytes. Hematoxylin-eosin staining (H&E) and Masson trichrome analysis were used to detect the kidney pathology in T2DN.
resultsThe levels of IL-6 and TNF-α were significantly increased in T2DN. p300 was significantly increased in T2DN. Consistently, p300 silencing significantly suppressed the inflammatory response and the overexpression of p300 significantly promoted the production of IL-6 and TNF-α in T2DN.
conclusionsThis study demonstrated that the production of IL-6 and TNF-α, and the expression of p300, were increased in T2DN. Furthermore, P300 significantly promoted the activation of the NF-κB subunit p65 through a direct association with p65 in T2DN, subsequently enhancing the production of IL-6 and TNF-α.
Indexed as
Identifiers
31934006PMC6947128W3026107616What 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.