ArticleBiochemical genetics2026
FTO Deficiency Inhibits Vascular Endothelial Cell Apoptosis and Improved Mitophagy in Obesity-Related Hypertension by Enhancing NDRG1 m6A Methylation.
Article in Biochemical genetics, 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular endothelial dysfunction contributes to obesity-related hypertension, yet its mechanisms remain unclear. This study examined the role of N6-methyladenosine (m6A) in this process using in vivo and in vitro models. C57BL/6J mice fed a high-fat diet (HFD) developed obesity-related hypertension, while oxidized low-density lipoprotein (ox-LDL)-treated human aortic endothelial cells (HAECs) simulated endothelial injury. Global m6A levels were assessed via dot blot, and m6A regulators were quantified by qPCR. Endothelial function was evaluated through viability (CCK-8), apoptosis (flow cytometry), and mitophagy (Western blot and immunofluorescence staining). Mechanistic studies included methylated RNA immunoprecipitation (MeRIP) and dual-luciferase assays. Results showed HFD reduced m6A levels but elevated Fto expression in mice, while ox-LDL decreased m6A levels and upregulated FTO in HAECs. FTO knockdown in HAECs enhanced viability and mitophagy while suppressing apoptosis under ox-LDL stress. Mechanistically, FTO silencing increased m6A methylation on NDRG1 mRNA, leading to its degradation via YTHDF2 recognition. NDRG1 overexpression reversed these effects, restoring apoptosis while reducing mitophagy and viability. These findings reveal that FTO depletion attenuates endothelial dysfunction in obesity-related hypertension by enhancing m6A-mediated suppression of NDRG1, highlighting the FTO/m6A/NDRG1/YTHDF2 axis as a therapeutic target for vascular protection.
Indexed as
Identifiers
42240709What Socratic 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 Socratic graph.