Evidence map›Paper›PMID 21318332›Full record

ArticleAge (Dordrecht, Netherlands)2012

Mechanism of Ang II involvement in activation of NF-κB through phosphorylation of p65 during aging.

Ji Min Kim, Hyoung-Sam Heo, Young Mi Ha, Byeong Hyeok Ye, Eun Kyeong Lee, Yeon Ja Choi, Byung Pal Yu, Hae Young Chung

Open access · bronzeAbstract read
In one paragraph

Article in Age (Dordrecht, Netherlands), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 15% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  13. Induced dysregulation of ACE2 by SARS-CoV-2 plays a key role in COVID-19 severity.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Aerobic exercise reverses arterial inflammation with aging in mice.American journal of physiology. Heart and circulatory physiology · 2011
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Ji Min KimMolecular Inflammation Research Center for Aging Intervention, Pusan National University, San 30, Jangjun-dong, Gumjung-gu, Busan, 609-735, South Korea.
Hyoung-Sam Heo
Young Mi Ha
Byeong Hyeok Ye
Eun Kyeong Lee
Yeon Ja Choi
Byung Pal Yu
Hae Young Chung
Pusan National University · KRThe University of Texas Health Science Center at San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin II (Ang II), a major effector of the renin-angiotensin system, is now recognized as a pro-inflammatory mediator. This Ang II signaling, which causes transcription of pro-inflammatory genes, is regulated through nuclear factor-κB (NF-κB). At present, the molecular mechanisms underlying the effect of aging on Ang II signaling and NF-κB activation are not fully understood. The purpose of this study was to document altered molecular events involved in age-related changes in Ang II signaling and NF-κB activation. Experimentations were carried out using kidney tissues from Fischer 344 rats at 6, 12, 18, and 24 months of age, and the rat endothelial cell line, YPEN-1 for the detailed molecular work. Results show that increases in Ang II and Ang II type 1 receptor during aging were accompanied by the generation of reactive species. Increased Ang II activated NF-κB by phosphorylating IκBα and p65. Increased phosphorylation of p65 at Ser 536 was mediated by the enhanced phosphorylation of IκB kinase αβ, while phosphorylation site Ser 276 of p65 was mediated by upregulated mitogen-activated and stress-activated protein kinase-1. These altered molecular events in aged animals were partly verified by experiments using YPEN-1 cells. Collectively, our findings provide molecular insights into the pro-inflammatory actions of Ang II, actions that influence the phosphorylation of p65-mediated NF-κB activation during aging. Our study demonstrates the age-related pleiotropic nature of the physiologically important Ang II can change into a deleterious culprit that contributes to an increased incidence of many chronic diseases such as atherosclerosis, diabetes, and dementia.

Indexed as

AgingAngiotensin IIAnimalsCell LineEndothelial CellsModels, AnimalNF-kappa BPhosphorylationRatsRats, Inbred F344Signal TransductionTranscription Factor RelAAngiotensin IINF-kappa BRela protein, ratTranscription Factor RelA

Identifiers

PMID21318332
PMCPMC3260361
OpenAlexW2087488450

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.