Evidence map›Paper›PMID 39776022›Full record

ReviewThe Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology2025

Hypertrophic cardiomyopathy: insights into pathophysiology and novel therapeutic strategies from clinical studies.

Samuel Oluwadare Olalekan, Olalekan Olanrewaju Bakare, Patrick Godwin Okwute, Ifabunmi Oduyemi Osonuga, Muinat Moronke Adeyanju, Victoria Biola Edema

Abstract readReview
In one paragraph

Review in The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

6 authors.

Samuel Oluwadare OlalekanDepartment of Physiology, Faculty of Basic Medical Sciences, Obafemi Awolowo College of Health Sciences, Olabisi Onabanjo University, Sagamu Campus, Sagamu, Ogun State, Nigeria. samuel.olalekan@oouagoiwoye.edu.ng.ORCID http://orcid.org/0000-0002-1329-0225
Olalekan Olanrewaju BakareDepartment of Biochemistry, Olabisi Onabanjo University, Sagamu Campus, Sagamu, Ogun State, Nigeria.
Patrick Godwin OkwuteDepartment of Physiology, Babcock University, Ilishan, Ogun State, Nigeria.
Ifabunmi Oduyemi OsonugaDepartment of Physiology, Faculty of Basic Medical Sciences, Obafemi Awolowo College of Health Sciences, Olabisi Onabanjo University, Sagamu Campus, Sagamu, Ogun State, Nigeria.
Muinat Moronke AdeyanjuDepartment of Biochemistry, Olabisi Onabanjo University, Sagamu Campus, Sagamu, Ogun State, Nigeria.
Victoria Biola EdemaDepartment of Physiology, Faculty of Basic Medical Sciences, Obafemi Awolowo College of Health Sciences, Olabisi Onabanjo University, Sagamu Campus, Sagamu, Ogun State, Nigeria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHypertrophic cardiomyopathy (HCM) is a frequently encountered cardiac condition worldwide, often inherited, and characterized by intricate phenotypic and genetic manifestations. The natural progression of HCM is diverse, largely due to mutations in the contractile and relaxation proteins of the heart. These mutations disrupt the normal structure and functioning of the heart muscle, particularly affecting genes that encode proteins involved in the contraction and relaxation of cardiac muscle. MAIN BODY: This review focused on understanding the role of contractile and relaxation proteins in the pathogenesis of hypertrophic cardiomyopathy. Mutations in contractile proteins such as myosin, actin, tropomyosin, and troponin are associated with hypercontractility and increased sensitivity of the heart muscle, leading to HCM. Additionally, impaired relaxation of the heart muscle, linked to abnormalities in proteins like phospholamban, sarcolipin, titin, myosin binding protein-C, and calsequestrin, contributes significantly to the disease. The review also explored the impact of targeted therapeutic approaches aimed at modulating these proteins to improve patient outcomes. Recent advances in therapeutic strategies, including novel pharmacological agents like mavacamten and aficamten, were examined for their potential to help patients manage the disease and lead more accommodating lifestyles.

conclusionsThe review underscored the significance of early diagnosis and personalized treatment approaches in managing HCM. Future research should prioritize the development of robust biomarkers for early detection and risk stratification, particularly in diverse populations, to enhance clinical outcomes. Furthermore, it is imperative to delve deeper into the genetic mutations and molecular mechanisms associated with HCM, with a focus on exploring the roles of less-studied myocardial relaxation proteins and their interactions with sarcomere constituents.

Indexed as

Cardiac myosin inhibitorsGenetic therapyHypertrophic cardiomyopathySarcomere proteins

Identifiers

PMID39776022
PMCPMC11706819

What Socratic 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 Socratic graph.