Evidence map›Paper›PMID 35011658›Full record

ArticleCells2021

Autophagy and Endoplasmic Reticulum Stress during Onset and Progression of Arrhythmogenic Cardiomyopathy.

Mark Pitsch, Sebastian Kant, Corinna Mytzka, Rudolf E Leube, Claudia A Krusche

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Targeting Autophagy in Atrial Fibrillation.Reviews in cardiovascular medicine · 2023
    Review
  12. Article
  13. Review
  14. 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.

Mark PitschInstitute of Molecular and Cellular Anatomy, RWTH Aachen University, Wendlingweg 2, 52074 Aachen, Germany.ORCID 0000-0003-3024-4463
Sebastian KantInstitute of Molecular and Cellular Anatomy, RWTH Aachen University, Wendlingweg 2, 52074 Aachen, Germany.
Corinna MytzkaInstitute of Molecular and Cellular Anatomy, RWTH Aachen University, Wendlingweg 2, 52074 Aachen, Germany.
Rudolf E LeubeInstitute of Molecular and Cellular Anatomy, RWTH Aachen University, Wendlingweg 2, 52074 Aachen, Germany.ORCID 0000-0002-5519-7379
Claudia A KruscheInstitute of Molecular and Cellular Anatomy, RWTH Aachen University, Wendlingweg 2, 52074 Aachen, Germany.ORCID 0000-0001-9914-9283
RWTH Aachen University · DE

Funding

Interdisciplinary Center for Clinical Research within the faculty of Medicine at Rheinisch-Westfälische Technische Hochschule Aachen University K7-4Interdisciplinary Center for Clinical Research within the faculty of Medicine at Rheinisch-Westfälische Technische Hochschule Aachen University T9-2START grant of the faculty of Medicine at Rheinisch-Westfälische Technische Hochschule Aachen University 30/18
6 · The paper itself

Abstract

Arrhythmogenic cardiomyopathy (AC) is a heritable, potentially lethal disease without a causal therapy. AC is characterized by focal cardiomyocyte death followed by inflammation and progressive formation of connective tissue. The pathomechanisms leading to structural disease onset and progression, however, are not fully elucidated. Recent studies revealed that dysregulation of autophagy and endoplasmic/sarcoplasmic reticulum (ER/SR) stress plays an important role in cardiac pathophysiology. We therefore examined the temporal and spatial expression patterns of autophagy and ER/SR stress indicators in murine AC models by qRT-PCR, immunohistochemistry, in situ hybridization and electron microscopy. Cardiomyocytes overexpressing the autophagy markers LC3 and SQSTM1/p62 and containing prominent autophagic vacuoles were detected next to regions of inflammation and fibrosis during onset and chronic disease progression. mRNAs of the ER stress markers Chop and sXbp1 were elevated in both ventricles at disease onset. During chronic disease progression Chop mRNA was upregulated in right ventricles. In addition, reduced Ryr2 mRNA expression together with often drastically enlarged ER/SR cisternae further indicated SR dysfunction during this disease phase. Our observations support the hypothesis that locally altered autophagy and enhanced ER/SR stress play a role in AC pathogenesis both at the onset and during chronic progression.

Indexed as

AutophagyEndoplasmic Reticulum StressAnimalsArrhythmias, CardiacAutophagosomesBiomarkersCalciumCardiomyopathiesChronic DiseaseDesmoglein 2Disease ProgressionMiceMice, KnockoutMicrotubule-Associated ProteinsMyocardiumMyocytes, CardiacBiomarkersCalciumDesmoglein 2Dsg2 protein, mouseMap1lc3b protein, mouseMicrotubule-Associated ProteinsNCX1 protein, mouseRNA, MessengerRyanodine Receptor Calcium Release ChannelSequestosome-1 ProteinSodium-Calcium ExchangerSqstm1 protein, mouseUbiquitinarrhythmogenic cardiomyopathyARVCautophagyChopdesmogleinER stress

Identifiers

PMID35011658
PMCPMC8750195
OpenAlexW4200575360

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.