Evidence map›Paper›PMID 34957257›Full record

ReviewFrontiers in cardiovascular medicine2021

miR-208a in Cardiac Hypertrophy and Remodeling.

Xing-Huai Huang, Jia-Lu Li, Xin-Yue Li, Shu-Xia Wang, Zhi-Han Jiao, Si-Qi Li, Jun Liu, Jian Ding

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Role of miRNA in Cardiovascular Diseases in Children-Systematic Review.International journal of molecular sciences · 2024
    Pooled it
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  14. Biomarkers in Heart Failure: A Review and a Wish.International journal of molecular sciences · 2025
    Review
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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 at 2 institutions in 1 country.

Xing-Huai HuangSchool of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
Jia-Lu LiSchool of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
Xin-Yue LiSchool of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
Shu-Xia WangSchool of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
Zhi-Han JiaoSchool of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
Si-Qi LiSchool of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
Jun LiuDepartment of Orthopaedics, Jiangsu Provincial Hospital of Traditional Chinese Medicine, Affiliated to Nanjing University of Chinese Traditional Medicine, Nanjing, China.
Jian DingSchool of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
Xi'an Jiaotong University · CNJiangsu Provincial Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Various stresses, including pressure overload and myocardial stretch, can trigger cardiac remodeling and result in heart diseases. The disorders are associated with high risk of morbidity and mortality and are among the major health problems in the world. MicroRNAs, a class of ~22nt-long small non-coding RNAs, have been found to participate in regulating heart development and function. One of them, miR-208a, a cardiac-specific microRNA, plays key role(s) in modulating gene expression in the heart, and is involved in a broad array of processes in cardiac pathogenesis. Genetic deletion or pharmacological inhibition of miR-208a in rodents attenuated stress-induced cardiac hypertrophy and remodeling. Transgenic expression of miR-208a in the heart was sufficient to cause hypertrophic growth of cardiomyocytes. miR-208a is also a key regulator of cardiac conduction system, either deletion or transgenic expression of miR-208a disturbed heart electrophysiology and could induce arrhythmias. In addition, miR-208a appeared to assist in regulating the expression of fast- and slow-twitch myofiber genes in the heart. Notably, this heart-specific miRNA could also modulate the "endocrine" function of cardiac muscle and govern the systemic energy homeostasis in the whole body. Despite of the critical roles, the underlying regulatory networks involving miR-208a are still elusive. Here, we summarize the progress made in understanding the function and mechanisms of this important miRNA in the heart, and propose several topics to be resolved as well as the hypothetical answers. We speculate that miR-208a may play diverse and even opposite roles by being involved in distinct molecular networks depending on the contexts. A deeper understanding of the precise mechanisms of its action under the conditions of cardiac homeostasis and diseases is needed. The clinical implications of miR-208a are also discussed.

Indexed as

cardiomyopathyhypertrophymiR-208amiRNASox6Trbp

Identifiers

PMID34957257
PMCPMC8695683
OpenAlexW4200273009

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.