ArticleJournal of molecular histology2026
Association of miR-671-3p expression with clinical efficacy and complications in hemodialysis patients.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular calcification (VC) is a common and severe complication in hemodialysis patients, increasing the risk of major adverse cardiovascular events (MACE). This study aimed to explore the clinical value of miR-671-3p in hemodialysis patients and its regulatory role in VC. A total of 163 end-stage renal disease (ESRD) patients undergoing hemodialysis were enrolled, including 107 with VC and 56 without VC. Clinical data were used to evaluate the role of miR-671-3p in the diagnosis (ROC) and risk prediction (logistic regression) of VC and MACE. A high-phosphorus-induced human aortic smooth muscle cells (hASMCs) calcification model was established, and then cell viability (CCK-8), apoptosis rate (flow cytometry), calcium content, alkaline phosphatase (ALP) activity, and the levels of Runx2 and α-SMA were measured. Bioinformatics analysis and a dual-luciferase assay were employed to predict and validate the downstream target genes of miR-671-3p. miR-671-3p was downregulated in VC patients and showed high diagnostic value for VC. Its levels showed significant correlations with disease severity and could effectively predict the risk of MACE in VC patients. Overexpression of miR-671-3p markedly alleviated calcification-induced decreases in cell viability, increases in apoptosis and calcium content, upregulation of ALP and Runx2, and downregulation of α-SMA; however, this protective effect was reversed by overexpression of its downstream target FBXW2. miR-671-3p may serve as a promising candidate biomarker for diagnosing VC and predicting MACE in VC patients. miR-671-3p may attenuate the progression of VC by inhibiting calcification in hASMCs.
Indexed as
Identifiers
42878744What OpenQuestion holds
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 OpenQuestion graph.