Evidence map›Paper›PMID 21856818›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011

Angiotensin II activates AMPK for execution of apoptosis through energy-dependent and -independent mechanisms.

Regina M Day, Young H Lee, Li Han, Yong-Chul Kim, Ying-Hong Feng

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  11. Angiotensin II: tapping the cell cycle machinery to kill endothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2012
    Article
  12. 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

5 authors at 1 institution in 1 country.

Regina M DayDept. of Pharmacology, Uniformed Services Univ. of the Health Sciences, 4301 Jones Bridge Rd., Bethesda, MD 20814-4799, USA. rday@usuhs.mil
Young H Lee
Li Han
Yong-Chul Kim
Ying-Hong Feng
Uniformed Services University of the Health Sciences · US

Funding

Inhibitory AT2 Receptor:Activation/Signaling MechanismsR01HL065492 · NHLBI · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI FENG, YING-HONG · 2002 to 2005
$1.2M
HGF Signaling in Pulmonary RemodelingR01HL073929 · NHLBI · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI DAY, REGINA M · 2004 to 2007
$1.0M
NHLBI NIH HHS HL065492NHLBI NIH HHS HL-073929NHLBI NIH HHS R01 HL065492NHLBI NIH HHS R01 HL073929
6 · The paper itself

Abstract

At the cellular level, 5'-AMP-activated protein kinase (AMPK) serves as a critical link between energy homeostasis and the regulation of fundamental biological activities, including apoptosis. Angiotensin (Ang) II plays a key role in fibrotic lung remodeling. We recently demonstrated that Ang II induces apoptosis in pulmonary artery endothelial cells (PAEC) through the Ang type 2 receptor (AT(2)). AT(2) activates Src-homology two-domain-containing phosphatase-2 (SHP-2) in a signaling cascade leading to Bcl-x(L) mRNA destabilization and initiation of intrinsic apoptosis. We investigated the requirement of AMPK and ATP generation for Ang II-induced apoptosis in PAEC. Ang II activated AMPK, which was required for ATP generation. Inhibition of ATP production by compound C, an AMPK inhibitor, or by oligomycin suppressed Ang II-induced apoptosis. Experiments in Chinese hamster ovary-K1 cells expressing ectopic AT(2) (wild-type, mutant D90A, or carboxy terminal truncated mutant tC319) demonstrated that AT(2) activation of AMPK required the active conformation of the receptor and the carboxy terminal 44 amino acids. AMPK associated with and activated SHP-2 and was required for Bcl-x(L) mRNA destabilization. These are the first findings demonstrating that AMPK is activated by Ang II to produce ATP required for apoptosis. Our data also indicate that AMPK plays an energy-independent role by mediating SHP-2 activation.

Indexed as

Adenosine TriphosphateAMP-Activated Protein KinasesAngiotensin IIAnimalsApoptosisbcl-X ProteinBlotting, WesternCattleCricetinaeCricetulusEndothelial CellsEnzyme ActivationMutationPlasmidsProtein Tyrosine Phosphatase, Non-Receptor Type 11Pulmonary ArteryAdenosine TriphosphateAMP-Activated Protein KinasesAngiotensin IIbcl-X ProteinProtein Tyrosine Phosphatase, Non-Receptor Type 11Receptor, Angiotensin, Type 2

Identifiers

PMID21856818
PMCPMC3213991
OpenAlexW2033212561

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.