Evidence map›Paper›PMID 27577254›Full record

ArticleScientific reports2016

Proliferation in cardiac fibroblasts induced by β1-adrenoceptor autoantibody and the underlying mechanisms.

Tingting Lv, Yunhui Du, Ning Cao, Suli Zhang, Yulin Gong, Yan Bai, Wen Wang, Huirong Liu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

33 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Tiliroside fromInternational journal of molecular sciences · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. cAMP Signalling Pathway in Biocontrol Fungi.Current issues in molecular biology · 2022
    Review
  13. Article
  14. Article
  15. Article
  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

8 authors at 1 institution in 1 country.

Tingting LvDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.
Yunhui DuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.
Ning CaoDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.
Suli ZhangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.
Yulin GongDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.
Yan BaiDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.
Wen WangDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.
Huirong LiuDepartment of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, PR China.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic sustained stimulation of β-adrenoceptor is closely related to cardiac fibrosis which is bad for cardiac function. Growing evidence showed that the high prevalence of β1-adrenoceptor autoantibody (β1-AA) in the sera of patients with various types of cardiovascular diseases decreased cardiac function. In the current study, we demonstrated that β1-AA impaired the cardiac function evaluated by echocardiography and that β1-AA triggered cardiac fibrosis in terms of increased expression of α-smooth muscle actin as the marker of myofibroblast and collagen deposition in a passive β1-AA immunized mice model during 16 weeks. Further, we showed that β1-AA activated β1-AR/cAMP/PKA pathway and promoted proliferation in primary cardiac fibroblasts through specific binding to β1-AR but not to β2-AR. Moreover, β1-AA was also likely to promote proliferation in cardiac fibroblasts through activating p38MAPK and ERK1/2 as p38MAPK inhibitor SB203580 and ERK1/2 inhibitor PD98059 partially reversed the proliferative effect. The persistent activating signalling of PKA and P38MAPK in 1 h induced by β1-AA was associated with lacking agonist-induced desensitization phenomena. The conditioned medium from β1-AA-stimulated cardiac fibroblasts induced cardiomyocyte apoptosis, which indicated that β1-AA changed the secretion of cardiac fibroblasts contributing to cardiac injury. These findings will contribute to our understanding of the pathological mechanisms of β1-AA.

Indexed as

ActinsAmino Acid SequenceAnimalsAnimals, NewbornAutoantibodiesCell LineCell ProliferationEchocardiographyEndomyocardial FibrosisFibroblastsFlavonoidsGene Expression RegulationImidazolesImmunization, PassiveMiceMice, Inbred BALB C2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneActa2 protein, ratActinsAutoantibodiesFlavonoidsImidazolesMapk1 protein, mouseMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3p38 Mitogen-Activated Protein KinasesPyridinesReceptors, Adrenergic, beta-1SB 203580

Identifiers

PMID27577254
PMCPMC5006240
OpenAlexW2511683895

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.