Evidence map›Paper›PMID 31744200›Full record

ReviewCells2019

Myocardial Adaptation in Pseudohypoxia: Signaling and Regulation of mPTP via Mitochondrial Connexin 43 and Cardiolipin.

Miroslav Ferko, Natália Andelová, Barbara Szeiffová Bačová, Magdaléna Jašová

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. The critical role of cardiolipin in metazoan differentiation, development, and maturation.Developmental dynamics : an official publication of the American Association of Anatomists · 2023
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Homocysteine and Mitochondria in Cardiovascular and Cerebrovascular Systems.International journal of molecular sciences · 2020
    Review
  13. Review
  14. Article
  15. 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

4 authors at 1 institution in 1 country.

Miroslav FerkoCenter of Experimental Medicine, Slovak Academy of Sciences, Institute for Heart Research, Dúbravská cesta 9, 841 04 Bratislava, Slovakia.
Natália AndelováCenter of Experimental Medicine, Slovak Academy of Sciences, Institute for Heart Research, Dúbravská cesta 9, 841 04 Bratislava, Slovakia.
Barbara Szeiffová BačováCenter of Experimental Medicine, Slovak Academy of Sciences, Institute for Heart Research, Dúbravská cesta 9, 841 04 Bratislava, Slovakia.
Magdaléna JašováCenter of Experimental Medicine, Slovak Academy of Sciences, Institute for Heart Research, Dúbravská cesta 9, 841 04 Bratislava, Slovakia.
Slovak Academy of Sciences · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Therapies intended to mitigate cardiovascular complications cannot be applied in practice without detailed knowledge of molecular mechanisms. Mitochondria, as the end-effector of cardioprotection, represent one of the possible therapeutic approaches. The present review provides an overview of factors affecting the regulation processes of mitochondria at the level of mitochondrial permeability transition pores (mPTP) resulting in comprehensive myocardial protection. The regulation of mPTP seems to be an important part of the mechanisms for maintaining the energy equilibrium of the heart under pathological conditions. Mitochondrial connexin 43 is involved in the regulation process by inhibition of mPTP opening. These individual cardioprotective mechanisms can be interconnected in the process of mitochondrial oxidative phosphorylation resulting in the maintenance of adenosine triphosphate (ATP) production. In this context, the degree of mitochondrial membrane fluidity appears to be a key factor in the preservation of ATP synthase rotation required for ATP formation. Moreover, changes in the composition of the cardiolipin's structure in the mitochondrial membrane can significantly affect the energy system under unfavorable conditions. This review aims to elucidate functional and structural changes of cardiac mitochondria subjected to preconditioning, with an emphasis on signaling pathways leading to mitochondrial energy maintenance during partial oxygen deprivation.

Indexed as

Adenosine TriphosphateCardiolipinsCell HypoxiaConnexin 43HumansMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreMyocardiumOxidative PhosphorylationSignal TransductionAdenosine TriphosphateCardiolipinsConnexin 43GJA1 protein, humanMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition Porecardiolipincardioprotectionmitochondriamitochondrial connexin 43mitochondrial permeability transition pores

Identifiers

PMID31744200
PMCPMC6912244
OpenAlexW2988853537

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.