Evidence map›Paper›PMID 23372925›Full record

ArticlePulmonary circulation2012

Cross talk between autophagy and apoptosis in pulmonary hypertension.

Yang Jin, Augustine M K Choi

Open access · bronzeAbstract read
In one paragraph

Article in Pulmonary circulation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

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  7. αJournal of personalized medicine · 2021
    Article
  8. Article
  9. The hallmarks of severe pulmonary arterial hypertension: the cancer hypothesis-ten years later.American journal of physiology. Lung cellular and molecular physiology · 2020
    Review
  10. 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.

Yang JinDivision of Pulmonary and Critical Care, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Augustine M K Choi
Brigham and Women's Hospital · US

Funding

Cross talk between cav-1 and flot1 in lung injuryR01HL102076 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI JIN, YANG · 2011 to 2015
$2.1M
NHLBI NIH HHS R01 HL102076
6 · The paper itself

Abstract

Endothelial cell (EC) apoptosis and apoptosis resistant proliferation have been proposed to play crucial roles in the development of featured plexiform lesions in the pathogenesis of pulmonary hypertension (PH). Subsequently, EC injury associated smooth muscle cell (SMC) proliferation facilitates vascular remodeling and eventually leads to narrowed vascular lumen, increased pulmonary vascular resistance, increased pulmonary arterial pressure, and right heart failure. The imbalance between cell death and proliferation occurs in every stage of pulmonary vascular remodeling and pathogenesis of PH, and involves every cell type in the vasculature including, but not limited to ECs, SMCs, and fibroblasts. Despite extensive studies, the detailed cellular and molecular mechanisms on how the transition from initial apoptosis of ECs to apoptosis resistant proliferation on ECs and SMCs remains unclear. Recent knowledge on autophagy, a conservative and powerful regulatory machinery existing in almost all mammalian cells, has shed light on the complex and delicate control on cell fate in the development of vascular remodeling in PH. In this review, we will discuss the recent understandings on how the cross-talk between apoptosis and autophagy regulates cell death or proliferation in PH pathogenesis, particularly in pulmonary vascular remodeling involving ECs and SMCs.

Indexed as

apoptosisautophagybeclin-1LC3pulmonary hypertension

Identifiers

PMID23372925
PMCPMC3555411
OpenAlexW2034849829

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.