The Oxidative Stress and Inflammatory Metabolic Pathways of Some Environmental Toxicants Inflicting Human Disorders
Toxics · Brimacombe M et al. · Paper published 22 Aug 2026
From the abstract
Numerous types of environmental toxicants alter human metabolomics, directly or indirectly, through gut microbial dysbiosis, upsetting immune homeostasis.
Shared under the paper’s CC BY licence.
The paper
The Oxidative Stress and Inflammatory Metabolic Pathways of Some Environmental Toxicants Inflicting Human Disorders
Brimacombe M, Lawrence DA
Toxics · 22 Aug 2026 · Peer-reviewed
- Relevance
- Relevant
- News value
- Routine
- Evidence
- Review
- Status
- Peer-reviewed
More on Inflammaging
See allCranial bone marrow monocytes drive brain injury inflammation and respond to fenofibrate
Targeting PPARα deficiency in cranial bone marrow monocytes improved cognitive function and reduced neurodegeneration markers in older patients with chronic brain injury.
Science translational medicine · Lu Z et al.
Somatic blood mutations associate with accelerated frailty and functional decline in humans
In a preprint analyzing over 730,000 adults, researchers linked clonal hematopoiesis to faster physical decline mediated by T-cell changes.
medRxiv · Zhao K et al.
Impaired glymphatic clearance links inflammation to accelerated brain aging in schizophrenia
Neuroimaging and post-mortem transcriptomics connect disrupted astrocytic aquaporin-4 polarization and blood-brain barrier breakdown to increased epigenetic and brain age.
bioRxiv · Tan X et al.
ASXL1 mutations in clonal hematopoiesis accelerate aortic valve calcification
Large human cohort data and cell experiments show that ASXL1-driven clonal hematopoiesis worsens aortic valve hemodynamics and promotes calcification through inflammatory signaling.
medRxiv · Small A et al.
Loss of SATB1 alters 3D genome architecture in aged mouse T cells
Declining levels of the chromatin organizer SATB1 disrupt genomic boundaries and drive inflammatory gene activation in naive CD4+ T cells.
Science advances · Wang B et al.