Evidence map›Paper›PMID 22508832›Full record

ArticleHypertension (Dallas, Tex. : 1979)2012

Left ventricular failure produces profound lung remodeling and pulmonary hypertension in mice: heart failure causes severe lung disease.

Yingjie Chen, Haipeng Guo, Dachun Xu, Xin Xu, Huan Wang, Xinli Hu, Zhongbing Lu, Dongmin Kwak, Yawei Xu, Roland Gunther and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 2 pooled it
8.1field-weighted citation impact, top 2% 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

82 citing papers in PubMed, 2 syntheses or guidelines pooled it, 152 citations in OpenAlex.

  1. Pooled it
  2. Guideline
  3. Trial
  4. Article
  5. Circular RNA circSmad4 controls pulmonary fibrosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Modeling HFpEF in animals.Nature cardiovascular research · 2025
    Article
  11. PHD2 Deletion in CD8Hypertension (Dallas, Tex. : 1979) · 2025
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. ALPK2 prevents cardiac diastolic dysfunction in heart failure with preserved ejection fraction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  20. Article

22 more citing papers are in PubMed but not listed here.

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

12 authors at 4 institutions in 2 countries.

Yingjie ChenLillehei Heart Institute and the Cardiovascular Division, University of Minnesota Medical School, Minneapolis, MN 55455, USA. chenx106@umn.edu
Haipeng Guo
Dachun Xu
Xin Xu
Huan Wang
Xinli Hu
Zhongbing Lu
Dongmin Kwak
Yawei Xu
Roland Gunther
Yuqing Huo
E Kenneth Weir
Qilu Hospital of Shandong University · CNShanghai Tenth People's Hospital · CNTongji University · CNUniversity of Minnesota · US

Funding

Opposing Modulation of K+ Channels by a Redox SensorR01HL065322 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI WEIR, EDWARD KENNETH · 2001 to 2008
$1.8M
Molecular mechanism of 4E-binding proteins on heart failure developmentR01HL105406 · NHLBI · UNIVERSITY OF MINNESOTA · PI CHEN, YINGJIE · 2011 to 2014
$1.5M
DDAH1 effects on endogenous NOS inhibitors and vascular endothelial functionR21HL098669 · NHLBI · UNIVERSITY OF MINNESOTA · PI CHEN, YINGJIE · 2010 to 2011
$415k
Regulation of the novel mTOR suppressor DDIT4 in the failing heartR21HL098719 · NHLBI · UNIVERSITY OF MINNESOTA · PI CHEN, YINGJIE · 2011 to 2012
$415k
DDAH1 effects on the development of congestive heart failureR21HL102597 · NHLBI · UNIVERSITY OF MINNESOTA · PI CHEN, YINGJIE · 2010 to 2011
$415k
NHLBI NIH HHS 1R01 HL079168NHLBI NIH HHS R01 HL065322NHLBI NIH HHS R01 HL105406NHLBI NIH HHS R01HL105406NHLBI NIH HHS R01HL65322NHLBI NIH HHS R21 HL098669NHLBI NIH HHS R21HL098669NHLBI NIH HHS R21 HL098719NHLBI NIH HHS R21HL098719NHLBI NIH HHS R21 HL102597NHLBI NIH HHS R21HL102597
6 · The paper itself

Abstract

Chronic left ventricular failure causes pulmonary congestion with increased lung weight and type 2 pulmonary hypertension. Understanding the molecular mechanisms for type 2 pulmonary hypertension and the development of novel treatments for this condition requires a robust experimental animal model and a good understanding of the nature of the resultant pulmonary remodeling. Here we demonstrate that chronic transverse aortic constriction causes massive pulmonary fibrosis and remodeling, as well as type 2 pulmonary hypertension, in mice. Thus, aortic constriction-induced left ventricular dysfunction and increased left ventricular end-diastolic pressure are associated with a ≤5.3-fold increase in lung wet weight and dry weight, pulmonary hypertension, and right ventricular hypertrophy. Interestingly, the aortic constriction-induced increase in lung weight was not associated with pulmonary edema but resulted from profound pulmonary remodeling with a dramatic increase in the percentage of fully muscularized lung vessels, marked vascular and lung fibrosis, myofibroblast proliferation, and leukocyte infiltration. The aortic constriction-induced left ventricular dysfunction was also associated with right ventricular hypertrophy, increased right ventricular end-diastolic pressure, and right atrial hypertrophy. The massive lung fibrosis, leukocyte infiltration, and pulmonary hypertension in mice after transverse aortic constriction clearly indicate that congestive heart failure also causes severe lung disease. The lung fibrosis and leukocyte infiltration may be important mechanisms in the poor clinical outcome in patients with end-stage heart failure. Thus, the effective treatment of left ventricular failure may require additional efforts to reduce lung fibrosis and the inflammatory response.

Indexed as

AnimalsAortaBlotting, WesternCollagenConstriction, PathologicFibrosisHeart FailureHypertension, PulmonaryHypertrophy, Left VentricularHypoxiaLeukocytesLungLung DiseasesMaleMiceMice, Inbred C57BLCollagenTransforming Growth Factor betaWater

Identifiers

PMID22508832
PMCPMC3402091
OpenAlexW2122594103

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.