Evidence map›Paper›PMID 26146467›Full record

ArticleCurrent topics in pharmacology2014

Molecular and cellular mechanisms of the inhibitory effects of ACE-2/ANG1-7/Mas axis on lung injury.

Indiwari Gopallawa, Bruce D Uhal

Open access · greenAbstract read
In one paragraph

Article in Current topics in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 30% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. E-Cigarette Vapour Increases ACE2 and TMPRSS2 Expression in a Flavour- and Nicotine-Dependent Manner.International journal of environmental research and public health · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. ACE2, Much More Than Just a Receptor for SARS-COV-2.Frontiers in cellular and infection microbiology · 2020
    Article
  12. Review
  13. 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

2 authors at 1 institution in 1 country.

Indiwari GopallawaDepartment of Biochemistry and Molecular Biology, Michigan State University, 3197 Biomedical and Physical Sciences Building, East Lansing, Michigan, 48824, USA.
Bruce D UhalDepartment of Physiology, Michigan State University, 3197 Biomedical and Physical Sciences Building, East Lansing, Michigan, 48824, USA.
Michigan State University · US

Funding

CONTROL OF TYPE II PNEUMOCYTE PROLIFERATIONR01HL045136 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI UHAL, BRUCE D · 1996 to 2012
$2.9M
NHLBI NIH HHS R01 HL045136
6 · The paper itself

Abstract

An established body of recent literature has demonstrated potent inhibitory effects of the angiotensin converting enzyme-2 (ACE-2)/ANG1-7/ Mas axis on acute lung injury and lung fibrogenesis. One of the mechanisms of this inhibition is the enzymatic action of ACE-2 to degrade its main substrate angiotensin (ANG) II, thereby reducing the injurious and profibrotic activities of this octapeptide. Another, potentially more important mechanism is the production by ACE-2 of the heptapeptide ANG1-7, which inhibits the actions of ANGII through its own receptor Mas, the product of the oncogene of the same name. Very recent efforts to define the molecular and cellular mechanisms of ANG1-7/Mas action have revealed a number of similar, but mechanistically distinct, pathways by which ANG1-7 and Mas act on various lung cell types to inhibit lung injury and fibrosis. In this review we summarize the beneficial actions of the ANG1-7/Mas pathway, specifically on lung cells in non-neoplastic lung injury. We also review the currently known downstream signaling mechanisms of the ANG1-7/Mas pathway in various lung cell types known to be key in acute injury and fibrogenesis.

Indexed as

ANG1-7apoptosislung injuryMassignaling

Identifiers

PMID26146467
PMCPMC4487538
OpenAlexW2407565284

What OpenQuestion holds

Textmetadata
LicenceTDM
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.