Article in Disease models & mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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.
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
7 authors.
Xiaoqiong FuDepartment of Cardiology, Children's Hospital of Chongqing Medical University, National Clinical Key Cardiovascular Specialty, National Clinical Research Center for Child Health and Disorders, Key Laboratory of Children's Important Organ Development and Diseases of Chongqing Municipal Health Commission, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Pediatrics, Chongqing Key Laboratory of Pediatrics, ChongQing 400014, China.ORCID 0009-0002-0193-7148
Wenjing YuanDepartment of Cardiology, Children's Hospital of Chongqing Medical University, National Clinical Key Cardiovascular Specialty, National Clinical Research Center for Child Health and Disorders, Key Laboratory of Children's Important Organ Development and Diseases of Chongqing Municipal Health Commission, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Pediatrics, Chongqing Key Laboratory of Pediatrics, ChongQing 400014, China.
Jiajin LiDepartment of Cardiology, Children's Hospital of Chongqing Medical University, National Clinical Key Cardiovascular Specialty, National Clinical Research Center for Child Health and Disorders, Key Laboratory of Children's Important Organ Development and Diseases of Chongqing Municipal Health Commission, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Pediatrics, Chongqing Key Laboratory of Pediatrics, ChongQing 400014, China.
Kun WanDepartment of Cardiology, Children's Hospital of Chongqing Medical University, National Clinical Key Cardiovascular Specialty, National Clinical Research Center for Child Health and Disorders, Key Laboratory of Children's Important Organ Development and Diseases of Chongqing Municipal Health Commission, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Pediatrics, Chongqing Key Laboratory of Pediatrics, ChongQing 400014, China.ORCID 0009-0001-5682-985X
Mei GeChongqing General Hospital, Chongqing University, Chongqing 400014, China.
Bo PanDepartment of Cardiology, Children's Hospital of Chongqing Medical University, National Clinical Key Cardiovascular Specialty, National Clinical Research Center for Child Health and Disorders, Key Laboratory of Children's Important Organ Development and Diseases of Chongqing Municipal Health Commission, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Pediatrics, Chongqing Key Laboratory of Pediatrics, ChongQing 400014, China.
Tiewei LuDepartment of Cardiology, Children's Hospital of Chongqing Medical University, National Clinical Key Cardiovascular Specialty, National Clinical Research Center for Child Health and Disorders, Key Laboratory of Children's Important Organ Development and Diseases of Chongqing Municipal Health Commission, Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing Key Laboratory of Pediatrics, Chongqing Key Laboratory of Pediatrics, ChongQing 400014, China.ORCID 0000-0002-0953-6552
Funding
Children's Hospital of Chongqing Medical UniversityChongqing Medical University w0176National Key Clinical Specialty Discipline Construction Program of China 010140National Natural Science Foundation of China 82170244
6 · The paper itself
Abstract
The rising incidence of cardiomyopathies poses a significant threat to the physical and mental health of patients. The establishment of an animal model that accurately reflects the clinicopathological characteristics of cardiomyopathy is essential for investigating its pathogenesis. In this study, a cardiomyocyte-specific Arhgef18 conditional knockout (cKO) mouse model was established with Cre/LoxP technology, and the results confirmed that the protein encoded by Arhgef18 (Rho/Rac guanine nucleotide exchange factor 18) was knocked out effectively in the myocardium of Arhgef18flox/flox; Nkx2.5-Cre (Arhgef18fl/fl cKO) mice. Compared to Arhgef18fl/fl mice, Arhgef18fl/fl cKO mice presented with slower body weight growth and no differences in survival curves. Cardiac structure and function revealed that Arhgef18fl/fl cKO mice developed biventricular enlargement, ventricular wall thinning and left-ventricular systolic dysfunction, along with increased Nppa and Nppb mRNA expression levels. Additionally, Arhgef18fl/fl cKO mice showed cardiomyocyte cytoskeletal rearrangements and cell polarity disorders. Our study results suggest that Arhgef18 cKO mice could provide an ideal animal model for the genetic investigation of cardiomyopathy.
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.
Establishment and functional studies of a model of cardiomyopathy with cardiomyocyte-specific conditional knockout of Arhgef18. · full record | OpenQuestion