Evidence map›Paper›PMID 32222157›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2020

CRISPR/Cas9-Mediated miR-29b Editing as a Treatment of Different Types of Muscle Atrophy in Mice.

Jin Li, Lijun Wang, Xuejiao Hua, Haifei Tang, Rui Chen, Tingting Yang, Saumya Das, Junjie Xiao

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

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  13. Advances in CRISPR therapeutics.Nature reviews. Nephrology · 2023
    Review
  14. Article
  15. Genome Editing to Abrogate Muscle Atrophy.Advances in experimental medicine and biology · 2023
    Review
  16. Article
  17. 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 2 countries.

Jin LiCardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China.
Lijun WangCardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China.
Xuejiao HuaCardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China.
Haifei TangCardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China.
Rui ChenCardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China.
Tingting YangCardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China.
Saumya DasCardiovascular Division of the Massachusetts General Hospital and Harvard Medical School, Boston, MA 02215, USA.
Junjie XiaoCardiac Regeneration and Ageing Lab, Institute of Cardiovascular Sciences, School of Life Science, Shanghai University, Shanghai 200444, China; School of Medicine, Shanghai University, Shanghai 200444, China. Electronic address: junjiexiao@shu.edu.cn.
Shanghai University · CNHarvard University · US

Funding

Novel Role for Circulating extracellular RNAs in Human Heart FailureR01HL122547 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI DAS, SAUMYA · 2015 to 2019
$2.1M
NHLBI NIH HHS R01 HL122547
6 · The paper itself

Abstract

Muscle atrophy is the loss of skeletal muscle mass and strength in response to diverse catabolic stimuli. At present, no effective treatments except exercise have been shown to reduce muscle atrophy clinically. Here, we report that CRISPR/Cas9-mediated genome editing through local injection into gastrocnemius muscles or tibialis anterior muscle efficiently targets the biogenesis processing sites in pre-miR-29b. In vivo, this CRISPR-based treatment prevented the muscle atrophy induced by angiotensin II (AngII), immobilization, and denervation via activation of the AKT-FOXO3A-mTOR signaling pathway and protected against AngII-induced myocyte apoptosis in mice, leading to significantly increased exercise capacity. Our work establishes CRISPR/Cas9-based gene targeting on miRNA as a potential durable therapy for the treatment of muscle atrophy and expands the strategies available interrogating miRNA function in vivo.

Indexed as

CRISPR-Cas SystemsAngiotensin IIAnimalsCRISPR-Associated Protein 9DependovirusDisease Models, AnimalGene EditingGenetic TherapyHEK293 CellsHumansImmobilizationInjections, IntramuscularMaleMiceMice, Inbred C57BLMicroRNAsAngiotensin IICRISPR-Associated Protein 9MicroRNAsMIRN29 microRNA, mouseRNA, Guide, CRISPR-Cas SystemsRNA, MessengerAKT-FOXO3A-mTOR signaling pathwayCRISPR/Cas9miR-29bmuscle atrophy

Identifiers

PMID32222157
PMCPMC7210721
OpenAlexW3010952107

What OpenQuestion holds

Textmetadata
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.