2026-10-14T08:38:40Z
https://api.figshare.com/v2/oai
oai:figshare.com:article/33990793
2026-09-24T20:08:26Z
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month_year_09_2026
Untargeted
Metabolomics for PM<sub>2.5</sub> Toxicity
in Rodent Models: A Systematic Review
Mengyao Wang (829984)
Xiaona Wang (662335)
Chenglei Qi (23066922)
Keke Long (22275280)
Shuling Duan (23634333)
Yingyang He (23688713)
Jiajun Xiao (22307069)
Shuyi Zhang (34553)
Yu Wang (12152)
Mu Zhu (62830)
Xiaoyan Yang (259084)
Qiong Wang (117288)
Yuanyuan Chen (165812)
Chao Wang (146527)
Wen Gu (129075)
Song Tang (586283)
Biochemistry
Medicine
Cell Biology
Genetics
Physiology
Biotechnology
Chemical Sciences not elsewhere classified
Biological Sciences not elsewhere classified
Cancer
standardized analytical workflows
specific metabolic alterations
relatively unbiased profiling
offers unique opportunities
mediated epigenetic dysregulation
g ., taurine
fine particulate matter
driven redox imbalance
complementary platform integration
276 unique exposure
linoleic acid metabolism
adverse health effects
5 </ sub
health concern
citric acid
untargeted metabolomics
throughput approach
systematic review
study comparisons
species validation
rodent models
provides global
pressing public
molecule metabolites
frequency metabolites
emerging contaminants
conventional approaches
associated metabolites
applicable framework
animal models
The adverse health effects of fine particulate matter
(PM<sub>2.5</sub>) remain a pressing public-health concern. Untargeted
metabolomics,
which provides global and relatively unbiased profiling of small-molecule
metabolites, offers unique opportunities to discover new exposure
biomarkers and clarify toxicity mechanisms beyond those of conventional
approaches. This systematic review synthesizes 42 untargeted metabolomics
studies in PM<sub>2.5</sub>-exposed rodent models. Integrative analysis
identifies 1,276 unique exposure-associated metabolites under the
predefined lenient screening criteria, with 24 high-frequency metabolites
(e.g., taurine, citric acid, alanine) and 31 recurrently perturbed
pathways (e.g., purine metabolism, linoleic acid metabolism, and tricarboxylic
acid cycle). These convergent alterations suggest three recurring
mechanistic themes: an energy-crisis-driven redox imbalance, oxidative-stress-mediated
epigenetic dysregulation, and inflammatory signaling via polyunsaturated
fatty acids. Tissue-specific metabolic alterations were prominent
in lungs (e.g., altered arachidonic acid), liver (e.g., purine catabolism),
and brain (e.g., lipid homeostasis disruption), demonstrating multiorgan
pathophysiological responses. Nevertheless, substantial methodological
heterogeneity across exposure protocols, animal models, and analytical
platforms complicates cross-study comparisons. These findings support
untargeted metabolomics as a high-throughput approach for characterizing
PM<sub>2.5</sub>-induced metabolic toxicity and offer an applicable
framework that may also inform studies of other emerging contaminants
and mixtures. Further progress will require more standardized analytical
workflows, complementary platform integration, and cross-species validation.
2026-09-24T00:00:00Z
Dataset
Dataset
10.1021/acs.chemrestox.6c00257.s003
https://figshare.com/articles/dataset/Untargeted_Metabolomics_for_PM_sub_2_5_sub_Toxicity_in_Rodent_Models_A_Systematic_Review/33990793
CC BY-NC 4.0