Evidence map›Paper›PMID 34205587›Full record

ReviewInternational journal of molecular sciences2021

From Genetic Mutations to Molecular Basis of Heart Failure Treatment: An Overview of the Mechanism and Implication of the Novel Modulators for Cardiac Myosin.

Yu-Jen Chen, Chian-Shiu Chien, Chern-En Chiang, Chen-Huan Chen, Hao-Min Cheng

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 14% 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

5 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Genetic Testing in Patients with Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2021
    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

5 authors at 2 institutions in 1 country.

Yu-Jen ChenDepartment of Internal Medicine, Division of Cardiovascular Medicine, Wan Fang Hospital, Taipei Medical University, Taipei 116081, Taiwan.ORCID 0000-0002-0231-4631
Chian-Shiu ChienInnovative Cellular Therapy Center, Department of Medical Research, Taipei Veterans General Hospital, Taipei 112201, Taiwan.ORCID 0000-0001-9666-1273
Chern-En ChiangGeneral Clinical Research Center, Taipei Veterans General Hospital, Taipei 112201, Taiwan.
Chen-Huan ChenDepartment of Medical Education, Taipei Veterans General Hospital, Taipei 112201, Taiwan.
Hao-Min ChengInstitute of Public Health, National Yang Ming Chiao Tung University, Taipei 112304, Taiwan.ORCID 0000-0002-3885-6600
National Yang Ming Chiao Tung University · TWTaipei Veterans General Hospital · TW

Funding

Ministry of Health and Welfare MOHW104-TDU-B-211-113-003, MOHW106-TDU-B-211-113001Ministry of Science and Technology MOST 106-2314-B-075 -051 -MY3, MOST 109-2314-B-010-061 -National Yang-Ming University E107F-M01-0501
6 · The paper itself

Abstract

Heart failure (HF) is a syndrome encompassing several important etiologies that lead to the imbalance between oxygen demand and supply. Despite the usage of guideline-directed medical therapy for HF has shown better outcomes, novel therapeutic strategies are desirable, especially for patients with preserved or mildly reduced left ventricular ejection fraction. In this regard, understanding the molecular basis for cardiomyopathies is expected to fill in the knowledge gap and generate new therapies to improve prognosis for HF. This review discusses an evolutionary mechanism designed to regulate cardiac contraction and relaxation through the most often genetically determined cardiomyopathies associated with HF. In addition, both the myosin inhibitor and myosin activator are promising new treatments for cardiomyopathies. A comprehensive review from genetic mutations to the molecular basis of direct sarcomere modulators will help shed light on future studies for a better characterization of HF etiologies and potential therapeutic targets.

Indexed as

Molecular Targeted TherapyBenzylaminesCardiac MyosinsHeart FailureHumansMyocytes, CardiacUracilUreaBenzylaminesCardiac MyosinsMYK-461omecamtiv mecarbilUracilUreacardiac myosindilated cardiomyopathyheart failurehereditary cardiomyopathyhypertrophic cardiomyopathy

Identifiers

PMID34205587
PMCPMC8234187
OpenAlexW3175112718

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.