ArticleNature communications2024
LncRNA-LncDACH1 mediated phenotypic switching of smooth muscle cells during neointimal hyperplasia in male arteriovenous fistulas.
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 9 papers.
What it found
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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.
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.
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Who cites it
9 citing papers in PubMed.
- Downregulation of the lncRNA PGM5P4-AS1 predicts poor prognosis and drives breast cancer progression through miR-3664-5p/KLF9.Cancer biology & therapy · 2026Article
- In search of LncDACH1 - a perceived intronic long non-coding RNA lacking fundamental genomic annotation evidence.Nature communications · 2026Article
- Porcine Skeletal Muscle-Specific lncRNA-ssc.37456 Regulates Myoblast Proliferation and Differentiation.Animals : an open access journal from MDPI · 2026Article
- Endothelial Klf9 fine-tunes Akt signaling to act as a transcriptional brake restraining retinal angiogenesis.International journal of biological sciences · 2026Article
- CLL, together with C1qR, suppresses WSSV infection by regulating the activation of Dorsal.Journal of virology · 2025Article
- Matrix metalloproteinase-3 promotes arteriovenous fistula failure by regulating FAK-AKT signaling.bioRxiv : the preprint server for biology · 2025Article
- Cellular and molecular mechanisms underlying hemodialysis arteriovenous fistula dysfunction and approaches to promote maturation: a vascular perspective.American journal of physiology. Heart and circulatory physiology · 2025Review
- Evaluating Animal Models for Improved Hemodialysis Vascular Access: A Focus on Arteriovenous Fistula.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Phenotypic switching of vascular smooth muscle cells: a central mechanism in vein graft intimal hyperplasia.Frontiers in cardiovascular medicine · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Arteriovenous fistulas (AVFs) are the most common vascular access points for hemodialysis (HD), but they have a high incidence of postoperative dysfunction, mainly due to excessive neointimal hyperplasia (NIH). Our previous studies have revealed a highly conserved LncRNA-LncDACH1 as an important regulator of cardiomyocyte and fibroblast proliferation. Herein, we find that LncDACH1 regulates NIH in AVF in male mice with conditional knockout of smooth muscle cell-specific LncDACH1 and in male mice model of AVF with LncDACH1 overexpression by adeno-associated virus. Mechanistically, silence of LncDACH1 activates p-AKT through promoting the expression of heat shock protein 90 (HSP90) and serine/arginine-rich splicing factor protein kinase 1 (SRPK1). Moreover, LncDACH1 is transcriptionally activated by transcription factor KLF9 that binds directly to the promoter region of the LncDACH1 gene. In this work, during AVF NIH, LncDACH1 is downregulated by KLF9 and promotes NIH through the HSP90/ SRPK1/ AKT signaling axis.
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Registered trials
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.