Evidence map›Paper›PMID 39766241›Full record

ReviewBiomolecules2024

Mitochondrial Dysfunction in Cardiac Disease: The Fort Fell.

Ioannis Paraskevaidis, Christos Kourek, Dimitrios Farmakis, Elias Tsougos

Abstract readReview
In one paragraph

Review in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. One Syndrome, Many Faces: A Unified Perspective on Heart Failure Phenotypes.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Review
  10. Exosome: an overview on enhanced biogenesis by small molecules.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  11. Review
  12. 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

4 authors.

Ioannis ParaskevaidisMedical School of Athens, National and Kapodistrian University of Athens, 15772 Athens, Greece.ORCID 0000-0002-7764-6411
Christos KourekMedical School of Athens, National and Kapodistrian University of Athens, 15772 Athens, Greece.ORCID 0000-0003-4348-2153
Dimitrios FarmakisMedical School of Athens, National and Kapodistrian University of Athens, 15772 Athens, Greece.ORCID 0000-0001-8364-3447
Elias TsougosDepartment of Cardiology, Hygeia Hospital, 15123 Athens, Greece.ORCID 0000-0001-9823-7564

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial cells and the extracellular matrix achieve their functions through the availability of energy. In fact, the mechanical and electrical properties of the heart are heavily dependent on the balance between energy production and consumption. The energy produced is utilized in various forms, including kinetic, dynamic, and thermal energy. Although total energy remains nearly constant, the contribution of each form changes over time. Thermal energy increases, while dynamic and kinetic energy decrease, ultimately becoming insufficient to adequately support cardiac function. As a result, toxic byproducts, unfolded or misfolded proteins, free radicals, and other harmful substances accumulate within the myocardium. This leads to the failure of crucial processes such as myocardial contraction-relaxation coupling, ion exchange, cell growth, and regulation of apoptosis and necrosis. Consequently, both the micro- and macro-architecture of the heart are altered. Energy production and consumption depend on the heart's metabolic resources and the functional state of the cardiac structure, including cardiomyocytes, non-cardiomyocyte cells, and their metabolic and energetic behavior. Mitochondria, which are intracellular organelles that produce more than 95% of ATP, play a critical role in fulfilling all these requirements. Therefore, it is essential to gain a deeper understanding of their anatomy, function, and homeostatic properties.

Indexed as

Energy MetabolismHeart DiseasesAdenosine TriphosphateAnimalsHumansMitochondriaMitochondria, HeartMyocardiumMyocytes, CardiacAdenosine Triphosphatecardiac diseaseenergyheart failuremitochondria

Identifiers

PMID39766241
PMCPMC11673776

What OpenQuestion holds

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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.