Evidence map›Paper›PMID 38782834›Full record

ArticleMolecular and cellular biochemistry2025

miR-486-5p diagnosed atrial fibrillation, predicted the risk of left atrial fibrosis, and regulated angiotensin II-induced cardiac fibrosis via modulating PI3K/Akt signaling through targeting FOXO1.

Fang Zhang, Lu Geng, Jing Zhang, Siliang Han, Mengya Guo, Yaxin Xu, Chunhong Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
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

7 authors.

Fang Zhang *Department of Cardiology, Affiliated Hospital of Hebei University, No. 212, Yuhua East Road, Baoding, 071000, People's Republic of China.
Lu Geng *Department of Cardiology, The Second Hospital of Hebei Medical University, Shijiazhuang, 050000, People's Republic of China.
Jing ZhangDepartment of Cardiology, Affiliated Hospital of Hebei University, No. 212, Yuhua East Road, Baoding, 071000, People's Republic of China.
Siliang HanDepartment of Cardiology, Affiliated Hospital of Hebei University, No. 212, Yuhua East Road, Baoding, 071000, People's Republic of China.
Mengya GuoDepartment of Cardiology, Affiliated Hospital of Hebei University, No. 212, Yuhua East Road, Baoding, 071000, People's Republic of China.
Yaxin XuDepartment of Cardiology, Affiliated Hospital of Hebei University, No. 212, Yuhua East Road, Baoding, 071000, People's Republic of China.
Chunhong ChenDepartment of Cardiology, Affiliated Hospital of Hebei University, No. 212, Yuhua East Road, Baoding, 071000, People's Republic of China. chenchunhongdr0312@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study focused on miR-486-5p in atrial fibrillation (AF) evaluating its clinical significance and revealing its regulatory mechanism in cardiac fibroblasts, aiming to explore a novel biomarker for AF. The study enrolled 131 AF patients and 77 non-AF individuals. With the help of polymerase chain reaction (PCR), the expression of miR-486-5p was evaluated. The significance of miR-486-5p in the diagnosis of AF and the occurrence of left atrial fibrosis (LAF) was assessed by receiver operating curve (ROC) and logistic analyses. The regulatory effect and mechanism of miR-486-5p on cardiac fibrosis were investigated in human cardiac fibroblasts treated with angiotensin II. miR-486-5p was significantly upregulated in AF patients and discriminated AF patients from non-AF individuals. Increasing miR-486-5p showed a significant association with decreasing left ventricular ejection fraction (LVEF), increasing left atrial diameter (LAD) and left ventricular end-diastolic diameter (LVEDd), and the high incidence of LAF in AF patients. Moreover, miR-486-5p was identified as a risk factor for LAF and could distinguish AF patients with LAF and without LAF. In cardiac fibroblasts, angiotensin II induced the upregulation of miR-486-5p and promoted cell proliferation, migration, and collagen synthesis. miR-486-5p negatively regulated forkhead box O1 (FOXO1) and its knockdown could reverse the promoted effect of angiotensin II. FOXO1 alleviated the effect of miR-486-5p, and the miR-486-5p/FOXO1 could activate PI3K/Akt signaling. The activation of PI3K/Akt signaling alleviated the enhanced proliferation, migration, and collagen synthesis of cardiac fibroblasts induced by angiotensin II, and its inhibition showed opposite effects. Increased miR-486-5p served as a biomarker for the diagnosis and development prediction of AF. miR-486-5p regulated cardiac fibroblast viability and collagen synthesis via modulating the PI3K/Akt signaling through targeting FOXO1.

Indexed as

Angiotensin IIAtrial FibrillationForkhead Box Protein O1Heart AtriaMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionAgedFemaleFibroblastsFibrosisHumansMaleMiddle AgedAngiotensin IIForkhead Box Protein O1FOXO1 protein, humanMicroRNAsMIRN486 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAtrial fibrillationAtrial fibrosisCardiac fibroblastsDiagnosismiRNA

Identifiers

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.