Evidence map›Paper›PMID 38892064›Full record

ArticleInternational journal of molecular sciences2024

Genetic Mutations and Mitochondrial Redox Signaling as Modulating Factors in Hypertrophic Cardiomyopathy: A Scoping Review.

Antonio da Silva Menezes Junior, Ana Luísa Guedes de França-E-Silva, Henrique Lima de Oliveira, Khissya Beatryz Alves de Lima, Iane de Oliveira Pires Porto, Thays Millena Alves Pedroso, Daniela de Melo E Silva, Aguinaldo F Freitas

Abstract readScoping Review
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

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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.

Antonio da Silva Menezes JuniorFaculdade de Medicina, Departamento de Clínica Médica, Universidade Federal de Goiás (UFG), Goiânia 74020-020, Brazil.ORCID 0000-0003-1751-5206
Ana Luísa Guedes de França-E-SilvaFaculdade de Medicina, Departamento de Clínica Médica, Universidade Federal de Goiás (UFG), Goiânia 74020-020, Brazil.ORCID 0000-0001-9001-1720
Henrique Lima de OliveiraFaculdade de Medicina, Departamento de Clínica Médica, Universidade Federal de Goiás (UFG), Goiânia 74020-020, Brazil.
Khissya Beatryz Alves de LimaFaculdade de Medicina, Departamento de Clínica Médica, Universidade Federal de Goiás (UFG), Goiânia 74020-020, Brazil.
Iane de Oliveira Pires PortoFaculdade de Medicina, Universidade de Rio Verde (UniRV), Campus Aparecida, Aparecida de Goiânia 74345-030, Brazil.ORCID 0000-0001-5153-1643
Thays Millena Alves PedrosoFaculdade de Medicina, Universidade de Rio Verde (UniRV), Campus Aparecida, Aparecida de Goiânia 74345-030, Brazil.ORCID 0000-0003-1224-7054
Daniela de Melo E SilvaFaculdade de Medicina, Departamento de Clínica Médica, Universidade Federal de Goiás (UFG), Goiânia 74020-020, Brazil.
Aguinaldo F FreitasFaculdade de Medicina, Departamento de Clínica Médica, Universidade Federal de Goiás (UFG), Goiânia 74020-020, Brazil.ORCID 0000-0003-3778-7153

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypertrophic cardiomyopathy (HCM) is a heart condition characterized by cellular and metabolic dysfunction, with mitochondrial dysfunction playing a crucial role. Although the direct relationship between genetic mutations and mitochondrial dysfunction remains unclear, targeting mitochondrial dysfunction presents promising opportunities for treatment, as there are currently no effective treatments available for HCM. This review adhered to the Preferred Reporting Items for Systematic Reviews and Meta-Analysis Extension for Scoping Reviews guidelines. Searches were conducted in databases such as PubMed, Embase, and Scopus up to September 2023 using "MESH terms". Bibliographic references from pertinent articles were also included. Hypertrophic cardiomyopathy (HCM) is influenced by ionic homeostasis, cardiac tissue remodeling, metabolic balance, genetic mutations, reactive oxygen species regulation, and mitochondrial dysfunction. The latter is a common factor regardless of the cause and is linked to intracellular calcium handling, energetic and oxidative stress, and HCM-induced hypertrophy. Hypertrophic cardiomyopathy treatments focus on symptom management and complication prevention. Targeted therapeutic approaches, such as improving mitochondrial bioenergetics, are being explored. This includes coenzyme Q and elamipretide therapies and metabolic strategies like therapeutic ketosis. Understanding the biomolecular, genetic, and mitochondrial mechanisms underlying HCM is crucial for developing new therapeutic modalities.

Indexed as

Cardiomyopathy, HypertrophicMutationOxidation-ReductionSignal TransductionAnimalsHumansMitochondriaOxidative StressReactive Oxygen SpeciesReactive Oxygen Specieshypertrophic cardiomyopathymetabolismmitochondrial dysfunctionmitochondrial redox signaling

Identifiers

PMID38892064
PMCPMC11173352

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.