Mitochondrial aldehyde dehydrogenase restores the migratory capacity inhibited by high glucose-induced hyperosmolality.

Chi-Cheng Huang, Yuh-Lien Chen, Chung-Liang Chien

Abstract read

In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing 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

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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

1 citing paper in PubMed.

The Multifaceted Role of Mitochondria in Angiogenesis.International journal of molecular sciences · 2025
Review

4 · The record

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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

3 authors.

Chi-Cheng HuangDivision of Cardiology, Cardiovascular Medical Center, Far Eastern Memorial Hospital, New Taipei City, Taiwan.

Yuh-Lien ChenGraduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan.

Chung-Liang ChienGraduate Institute of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan. chien@ntu.edu.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cell migration, which is often impaired under high glucose (HG) conditions, plays a crucial role in the pathogenesis of various diabetic complications. This study investigates the role of mitochondrial aldehyde dehydrogenase (ALDH2) in the HG-induced migratory inhibition. Using fibroblasts sub-cultured in HG medium as a cell model of chronic hyperglycemia, we found that prolonged exposure to HG stress inhibited cell migration via a novel mechanism independent of oxidative stress or cell death. By increasing osmolality, HG induced perinuclear clustering of mitochondria, enhanced focal adhesion maturation, and caused the cells to be less responsive to migratory cues. The pharmacological inhibition of ALDH2 exaggerated this phenomenon, while ALDH2 overexpression protected cells from the migratory impairment caused by HG-induced hyperosmolality. Cells with ALDH2 overexpression exhibited less mature focal adhesions and longer mitochondrial network, suggesting that ALDH2 might preserve mitochondrial integrity to facilitate the focal adhesion turnover during cell migration.

Indexed as

Aldehyde Dehydrogenase, MitochondrialCell MovementGlucoseMitochondriaAnimalsCell LineFibroblastsFocal AdhesionsHumansMiceOsmolar ConcentrationAldehyde Dehydrogenase, MitochondrialALDH2 protein, humanGlucoseAldehyde dehydrogenaseCell migrationCytoskeletonFocal adhesionHyperglycemiaHyperosmolalityMitochondria

Identifiers

PMID40404697

DOI10.1038/s41598-025-02022-x

PMCPMC12098716

What Socratic holds

Textmetadata

LicenceCC BY-NC-ND

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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.