Evidence map›Paper›PMID 39143095›Full record

ArticleNature communications2024

Lamin A/C deficiency-mediated ROS elevation contributes to pathogenic phenotypes of dilated cardiomyopathy in iPSC model.

Hangyuan Qiu, Yaxun Sun, Xiaochen Wang, Tingyu Gong, Jun Su, Jiaxi Shen, Jingjun Zhou, Jiafeng Xia, Hao Wang, Xiangfu Meng and 4 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
–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

27 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. [Advances in the molecular genetics of nuclear gene mutations causing pediatric mitochondrial cardiomyopathy].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Pooled it
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  9. RNA-Based Therapies for Treating Monogenic Cardiomyopathies.The Canadian journal of cardiology · 2026
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  13. Metabolic Reprogramming Driven by Trophoblasts and Decidual XCR1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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.

Hangyuan QiuDepartment of Cardiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Yaxun SunDepartment of Cardiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Xiaochen WangKey Laboratory of combined Multi-organ Transplantation, Ministry of Public Health, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Tingyu GongKey Laboratory of combined Multi-organ Transplantation, Ministry of Public Health, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Jun SuKey Laboratory of combined Multi-organ Transplantation, Ministry of Public Health, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Jiaxi ShenKey Laboratory of combined Multi-organ Transplantation, Ministry of Public Health, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-6540-8283
Jingjun ZhouKey Laboratory of combined Multi-organ Transplantation, Ministry of Public Health, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Jiafeng XiaState Key Laboratory for Diagnosis and Treatment of Infectious Diseases, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Hao WangPrenatal Diagnosis Center, Hangzhou Women's Hospital, Hangzhou, China.
Xiangfu MengState Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Science, Hubei University, Wuhan, China.
Guosheng FuDepartment of Cardiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Donghui ZhangState Key Laboratory of Biocatalysis and Enzyme Engineering, School of Life Science, Hubei University, Wuhan, China.
Chenyang JiangDepartment of Cardiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China. cyjiang@zju.edu.cn.
Ping LiangKey Laboratory of combined Multi-organ Transplantation, Ministry of Public Health, the First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China. pingliang@zju.edu.cn.ORCID 0000-0001-6806-3735

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81870175National Natural Science Foundation of China (National Science Foundation of China) 81922006National Natural Science Foundation of China (National Science Foundation of China) 82370313National Natural Science Foundation of China (National Science Foundation of China) 82370354
6 · The paper itself

Abstract

Mutations in the nuclear envelope (NE) protein lamin A/C (encoded by LMNA), cause a severe form of dilated cardiomyopathy (DCM) with early-onset life-threatening arrhythmias. However, molecular mechanisms underlying increased arrhythmogenesis in LMNA-related DCM (LMNA-DCM) remain largely unknown. Here we show that a frameshift mutation in LMNA causes abnormal Ca

Indexed as

Cardiomyopathy, DilatedInduced Pluripotent Stem CellsLamin Type AMyocytes, CardiacOxidative StressReactive Oxygen SpeciesSirtuin 1Arrhythmias, CardiacCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Frameshift MutationHumansMaleMicrotubule-Associated ProteinsMitochondriaNuclear EnvelopeCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Lamin Type ALMNA protein, humanMicrotubule-Associated ProteinsReactive Oxygen SpeciesRyanodine Receptor Calcium Release ChannelSIRT1 protein, humanSirtuin 1

Identifiers

PMID39143095
PMCPMC11324749

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.