Evidence map›Paper›PMID 35089423›Full record

ArticleCellular and molecular life sciences : CMLS2022

PRMT7 ablation in cardiomyocytes causes cardiac hypertrophy and fibrosis through β-catenin dysregulation.

Byeong-Yun Ahn, Myong-Ho Jeong, Jung-Hoon Pyun, Hyeon-Ju Jeong, Tuan Anh Vuong, Ju-Hyeon Bae, Subin An, Su Woo Kim, Yong Kee Kim, Dongryeol Ryu and 4 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

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  14. Amino acid metabolism in health and disease.Signal transduction and targeted therapy · 2023
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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

14 authors at 4 institutions in 2 countries.

Byeong-Yun Ahn *Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, 2066, Seobu-Ro, Jangan-gu, Suwon, 16419, Gyeonggi-do, Republic of Korea.
Myong-Ho Jeong *Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, 2066, Seobu-Ro, Jangan-gu, Suwon, 16419, Gyeonggi-do, Republic of Korea.
Jung-Hoon PyunDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, 2066, Seobu-Ro, Jangan-gu, Suwon, 16419, Gyeonggi-do, Republic of Korea.
Hyeon-Ju JeongDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, 2066, Seobu-Ro, Jangan-gu, Suwon, 16419, Gyeonggi-do, Republic of Korea.
Tuan Anh VuongDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, 2066, Seobu-Ro, Jangan-gu, Suwon, 16419, Gyeonggi-do, Republic of Korea.
Ju-Hyeon BaeDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, 2066, Seobu-Ro, Jangan-gu, Suwon, 16419, Gyeonggi-do, Republic of Korea.
Subin AnDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, 2066, Seobu-Ro, Jangan-gu, Suwon, 16419, Gyeonggi-do, Republic of Korea.
Su Woo KimDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, 2066, Seobu-Ro, Jangan-gu, Suwon, 16419, Gyeonggi-do, Republic of Korea.
Yong Kee KimDrug Information Research Institute, College of Pharmacy, Sookmyung Women's University, 100 Cheongpa-ro 47-gil, Seoul, 04310, Republic of Korea.
Dongryeol RyuDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, 2066, Seobu-Ro, Jangan-gu, Suwon, 16419, Gyeonggi-do, Republic of Korea.
Hyun-Ji KimDepartment of Physiology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea.
Hana ChoDepartment of Physiology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea.
Gyu-Un BaeDrug Information Research Institute, College of Pharmacy, Sookmyung Women's University, 100 Cheongpa-ro 47-gil, Seoul, 04310, Republic of Korea. gbae@sookmyung.ac.kr.ORCID http://orcid.org/0000-0003-4262-1895
Jong-Sun KangDepartment of Molecular Cell Biology, Sungkyunkwan University School of Medicine, 2066, Seobu-Ro, Jangan-gu, Suwon, 16419, Gyeonggi-do, Republic of Korea. kangj01@skku.edu.
Sungkyunkwan University · KRSookmyung Women's University · KRInstitute of Aging · CAKorea National Institute of Health · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin II (AngII) has potent cardiac hypertrophic effects mediated through activation of hypertrophic signaling like Wnt/β-Catenin signaling. In the current study, we examined the role of protein arginine methyltransferase 7 (PRMT7) in cardiac function. PRMT7 was greatly decreased in hypertrophic hearts chronically infused with AngII and cardiomyocytes treated with AngII. PRMT7 depletion in rat cardiomyocytes resulted in hypertrophic responses. Consistently, mice lacking PRMT7 exhibited the cardiac hypertrophy and fibrosis. PRMT7 overexpression abrogated the cellular hypertrophy elicited by AngII, while PRMT7 depletion exacerbated the hypertrophic response caused by AngII. Similar with AngII treatment, the cardiac transcriptome analysis of PRMT7-deficient hearts revealed the alteration in gene expression profile related to Wnt signaling pathway. Inhibition of PRMT7 by gene deletion or an inhibitor treatment enhanced the activity of β-catenin. PRMT7 deficiency decreases symmetric dimethylation of β-catenin. Mechanistic studies reveal that methylation of arginine residue 93 in β-catenin decreases the activity of β-catenin. Taken together, our data suggest that PRMT7 is important for normal cardiac function through suppression of β-catenin activity.

Indexed as

AngiotensinsAnimalsbeta CateninCardiomegalyFibrosisGene Expression ProfilingHumansMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMyocardiumMyocytes, CardiacProtein-Arginine N-MethyltransferasesRNA-SeqAngiotensinsbeta CateninPRMT7 protein, mouseProtein-Arginine N-MethyltransferasesCardiomyopathyPRMT7Wntβ-catenin

Identifiers

PMID35089423
PMCPMC11071781
OpenAlexW4221029553

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.