Evidence map›Paper›PMID 32503464›Full record

ArticleBMC cardiovascular disorders2020

β1 adrenoceptor antibodies induce myocardial apoptosis via inhibiting PGC-1α-related pathway.

Linying Shi, Jia Liu, Yuan Zhang, Mulei Chen, Jiamei Liu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cardiovascular disorders, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.7field-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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Targeting Adrenergic Receptors in Metabolic Therapies for Heart Failure.International journal of molecular sciences · 2021
    Review
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.

Linying ShiHeart Failure Center, Department of Cardiology, Beijing Chao-Yang Hospital, Capital Medical University, 8 Gongrentiyuchangnan Rd, Beijing, 100020, China.
Jia LiuHeart Failure Center, Department of Cardiology, Beijing Chao-Yang Hospital, Capital Medical University, 8 Gongrentiyuchangnan Rd, Beijing, 100020, China.
Yuan ZhangHeart Failure Center, Department of Cardiology, Beijing Chao-Yang Hospital, Capital Medical University, 8 Gongrentiyuchangnan Rd, Beijing, 100020, China.
Mulei ChenHeart Failure Center, Department of Cardiology, Beijing Chao-Yang Hospital, Capital Medical University, 8 Gongrentiyuchangnan Rd, Beijing, 100020, China. cml1968@sina.com.
Jiamei LiuHeart Failure Center, Department of Cardiology, Beijing Chao-Yang Hospital, Capital Medical University, 8 Gongrentiyuchangnan Rd, Beijing, 100020, China. liujiamei2006@yeah.net.ORCID 0000-0003-2241-3116
Capital Medical University · CN

Funding

National Science Foundation of China 81471477
6 · The paper itself

Abstract

backgroundPeripartum cardiomyopathy (PPCM) is life-threatening heart disease. However, the causes and pathogenesis of PPCM remain unclear. Previous studies found that β1 adrenoceptor antibodies (β1AA) had possible involvement in the development of PPCM. In the present study, we determined the potential relationship between PPCM and β1AA, including the mechanism of β1AA leading to PPCM.

methodsWe extracted the β1AA from the postpartum Wistar rats that were injected by the antigen peptide segment of the β1 adrenoceptor to produce PPCM. We tested the effects of β1AA on H9C2 cell line by CCK-8, LDH, TUNEL, SA-ELISA, qRT-PCR, and western blot methods. Furthermore, PGC-1α was overexpressed to rescue the effect of β1AA on H9C2 cells.

resultsWe found that the extracted β1AA induced apoptosis of cardiac myocytes of H9C2 cell line. Moreover, the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), which is a master regulator of mitochondrial metabolism, and its downstream transcript vascular endothelial growth factor (VEGF) got decreased in H9C2 cells after β1AA treatment. In addition, the effect of β1AA could be inhibited by atenolol, the antagonist of β1 adrenoceptors (β1AR) and imitated by isoprenaline, the agonist of β1AR. Furthermore, overexpression of PGC-1α in the H9C2 cells rescued the apoptosis of cells and inhibitory expression of VEGF induced by β1AA.

conclusionsOur results suggest that the symptoms of PPCM due to myocardial cell apoptosis induced by β1AA inhibiting the PGC-1α-related pathway impairs mitochondrial energy metabolism. Therefore, our results uncover a previously unknown role of the β1AA pathway in the etiology of PPCM and provide a novel potential target for the treatment of PPCM.

Indexed as

ApoptosisAnimalsAntibodiesCardiomyopathiesCell LineFemaleMyocytes, CardiacPeripartum PeriodPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPregnancyPregnancy Complications, CardiovascularRats, WistarReceptors, Adrenergic, beta-1Signal TransductionVascular Endothelial Growth Factor AAdrb1 protein, ratAntibodiesPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratReceptors, Adrenergic, beta-1Vascular Endothelial Growth Factor Avascular endothelial growth factor A, ratApoptosisAutoantibody against β1 adrenoceptorPeripartum cardiomyopathyPeroxisome proliferator-activated receptor γ coactivator-1αVascular endothelial growth factor

Identifiers

PMID32503464
PMCPMC7275518
OpenAlexW3034079706

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Registered trials

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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.