Evidence map›Paper›PMID 18557800›Full record

ReviewJournal of gastroenterology and hepatology2008

Liver disease and the renin-angiotensin system: recent discoveries and clinical implications.

John S Lubel, Chandana B Herath, Louise M Burrell, Peter W Angus

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of gastroenterology and hepatology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. The Renin-Angiotensin System in Liver Disease.International journal of molecular sciences · 2024
    Review
  8. [Hemodynamic Changes in Chronic Liver Disease].The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi · 2023
    Review
  9. Article
  10. Vitamin D improves hepatic alterations inSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Article
  11. Article
  12. Article
  13. Effects of PM2.5 Exposure on the ACE/ACE2 Pathway: Possible Implication in COVID-19 Pandemic.International journal of environmental research and public health · 2023
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

4 authors at 2 institutions in 1 country.

John S LubelDepartment of Medicine, The University of Melbourne, Austin and Northern Health, Melbourne, Victoria, Australia.
Chandana B Herath
Louise M Burrell
Peter W Angus
Northern Health · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The renin-angiotensin system (RAS) is a key regulator of vascular resistance, sodium and water homeostasis and the response to tissue injury. Historically, angiotensin II (Ang II) was thought to be the primary effector peptide of this system. Ang II is produced predominantly by the effect of angiotensin converting enzyme (ACE) on angiotensin I (Ang I). Ang II acts mainly through the angiotensin II type-1 receptor (AT(1)) and, together with ACE, these components represent the 'classical' axis of the RAS. Drug therapies targeting the RAS by inhibiting Ang II formation (ACE inhibitors) or binding to its receptor (angiotensin receptor blockers) are now in widespread clinical use and have been shown to reduce tissue injury and fibrosis in cardiac and renal disease independently of their effects on blood pressure. In 2000, two groups using different methodologies identified a homolog of ACE, called ACE2, which cleaves Ang II to form the biologically active heptapeptide, Ang-(1-7). Conceptually, ACE2, Ang-(1-7), and its putative receptor, the mas receptor represent an 'alternative' axis of the RAS capable of opposing the often deleterious actions of Ang II. Interestingly, ACE inhibitors and angiotensin receptor blockers increase Ang-(1-7) production and it has been proposed that some of the beneficial effects of these drugs are mediated through upregulation of Ang-(1-7) rather than inhibition of Ang II production or receptor binding. The present review focuses on the novel components and pathways of the RAS with particular reference to their potential contribution towards the pathophysiology of liver disease.

Indexed as

Renin-Angiotensin SystemAngiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsAngiotensin IAngiotensin IIAngiotensin II Type 1 Receptor BlockersAngiotensinsAnimalsHumansHypertension, PortalKallikreinsKininsLiverLiver CirrhosisLiver DiseasesPeptide FragmentsACE2 protein, humanAngiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsAngiotensin Iangiotensin I (1-7)Angiotensin IIAngiotensin II Type 1 Receptor BlockersAngiotensinsKallikreinsKininsPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupled

Identifiers

PMID18557800
PMCPMC7166336
OpenAlexW2169843939

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.