Evidence map›Paper›PMID 42281927›Full record

ArticleMechanobiology in medicine2026

Mechanosensitive reactive oxygen Species:A precision medicine target for oxidative stress-related diseases.

Kai Huang

Abstract read
In one paragraph

Article in Mechanobiology in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Kai HuangInstitute of Mechanobiology & Medical Engineering, School of Life Sciences & Biotechnology, Shanghai Jiao Tong University, 800 Dongchuan Road, Minhang, 200240, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress induced by abnormal mechanical stress is a common pathological mechanism underlying the initiation and progression of various injury and diseases. Mechanosensitive reactive oxygen species (mechano-ROS), a subset of ROS specifically elicited by mechanical stress, are primarily generated from distinct sources including NADPH oxidases (NOXs), mitochondrial electron transport chain (ETC), uncoupled endothelial nitric oxide synthase (eNOS), and xanthine oxidase (XO/XOR) in a disease-specific manner. These mechano-ROS act as critical signaling mediators that link aberrant mechanical cues to cellular dysfunction, inflammation, barrier disruption, and disease progression. Scavenging excessive reactive oxygen species (ROS) has thus emerged as a key strategy for mitigating injury and disease progression. However, the primary enzymatic systems and cellular sources responsible for ROS generation differ across diseases, which may partly account for the limited clinical efficacy of broad-spectrum antioxidant therapies. Consequently, targeted interventions that identify and inhibit disease-specific major ROS sources, in combination with ROS-scavenging strategies, could synergistically reduce oxidative stress by both upstream source suppression and downstream ROS clearance. This approach offers promising avenues for the precision attenuation/treatment of different injury and diseases.

Indexed as

Endothelial nitric oxide synthase (eNOS)Mechanical stressMitochondrial ROS (mtROS)NADPH oxidase (NOX)Oxidative stressReactive oxygen species (ROS)

Identifiers

PMID42281927
PMCPMC13251198

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.