Evidence map›Paper›PMID 18090668›Full record

ReviewCurrent opinion in nephrology and hypertension2008

Nuclear factor-kappaB as a hormonal intracellular signaling molecule: focus on angiotensin II-induced cardiovascular and renal injury.

Xiao C Li, Jia L Zhuo

Abstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

32 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Angiotensin II and ATInternational journal of molecular sciences · 2022
    Review
  5. Apela inhibits systemic and renal inflammatory reactions in mice with type I cardiorenal syndrome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  6. Review
  7. Review
  8. Review
  9. SARS-CoV-2-mediated inflammatory response in lungs: should we look at RAGE?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
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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

2 authors at 1 institution in 1 country.

Xiao C LiLaboratory of Receptor and Signal Transduction, Division of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Hospital, and Department of Physiology, Wayne State University School of Medicine, Detroit, Michigan 48202, USA.
Jia L Zhuo
Henry Ford Hospital · US

Funding

Role of Intracrine Angiotensin II in Kidney CellsR01DK067299 · NIDDK · UNIVERSITY OF MISSISSIPPI MED CTR · PI Jia Long Zhuo · 2004 to 2026
$6.5M
NIDDK NIH HHS 5R01DK067299NIDDK NIH HHS R01 DK067299
6 · The paper itself

Abstract

purpose of reviewNuclear factor-kappaB (NF-kappaB) has recently emerged as a novel intracellular signaling molecule for hormones, cytokines, chemokines, and growth factors. The purpose of this article is to highlight the role of NF-kappaB as an intracellular signaling for angiotensin II and clinical perspectives of targeting NF-kappaB signaling in treating hypertensive and renal diseases. RECENT

findingsA selective review of recently published work provides strong evidence that activation of NF-kappaB signaling by angiotensin II mediates the detrimental effects of angiotensin II on the transcription of cytokines, chemokines and growth factors. Angiotensin II stimulates AT1 receptors to activate NF-kappaB signaling via both canonical (classical) and noncanonical (alternative) pathways. Intracellular angiotensin II may also induce NF-kappaB activation and transactivation of target genes. Nearly 800 NF-kappaB inhibitors have been described, but none has advanced to clinical trials. However, angiotensin converting enzyme inhibitors and AT1 blockers are beneficial in treating angiotensin II-induced hypertensive and renal injury in part by inhibiting NF-kappaB activation. SUMMARY: Angiotensin II induces the transcription of cytokines, chemokines and growth factors, leading to target organ injury. These responses to angiotensin II are caused primarily by AT1 receptor-activated NF-kappaB signaling. Targeting NF-kappaB signaling with angiotensin converting enzyme inhibitors, AT1 blockers, and specific NF-kappaB inhibitors may represent a novel approach in treating angiotensin II-induced hypertensive and renal diseases.

Indexed as

Signal TransductionAngiotensin IIAnimalsCardiovascular DiseasesHumansKidney DiseasesNF-kappa BAngiotensin IINF-kappa B

Identifiers

PMID18090668
PMCPMC2278240
OpenAlexW1994814979

What OpenQuestion holds

Textmetadata
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.