Transparent minispheres reveal that some look-alike cancer drugs part ways in 3D
Peer-Reviewed Publication
Updates every hour. Last Updated: 28-Oct-2026 19:16 ET (28-Oct-2026 23:16 GMT/UTC)
Mitochondrial oxidative stress — the imbalance between mitochondrial reactive oxygen species (ROS) generation and their elimination — has emerged as a shared feature of autoimmune disease, but its mechanisms and the barriers to treating it differ substantially between conditions. A narrative review published in Medicine Discovery examines rheumatoid arthritis, systemic lupus erythematosus and multiple sclerosis, integrating five regulatory pathways that maintain mitochondrial redox homeostasis (NRF2/KEAP1-ARE, AMPK/SIRT1/PGC-1α, SIRT3-mediated deacetylation, mitophagy, and the inflammasome) into a single network in which the adaptor p62/SQSTM1 couples mitophagy to NRF2 activation and the NAD+ pool jointly controls SIRT1 in the nucleus and SIRT3 in mitochondria. The review traces a bidirectional loop: oxidized mitochondrial DNA released into the cytoplasm triggers type I interferon signalling through cGAS-STING and is sensed by TLR9 in plasmacytoid dendritic cells, while mitochondrial components including cardiolipin and oxidized mitochondrial DNA can serve as autoantigens; in the reverse direction, TNF-α and IFN-γ inhibit the electron transport chain and increase ROS leakage, and regulatory T cell function is impaired. Disease-specific mechanisms are compared — a Warburg-type metabolic shift in rheumatoid arthritis synovial fibroblasts, defective mitophagy with interferon activation in lupus, and oligodendrocyte energy failure with blood-brain barrier disruption in multiple sclerosis. Therapeutic strategies reviewed include mitochondria-targeted antioxidants (MitoQ, SS-31), natural antioxidants, antioxidant nanoparticles, NOX4 and NLRP3 inhibitors, mitophagy regulators, and metabolic reprogramming, with the caveat that ROS also carry essential physiological signalling roles. The authors emphasise that agents targeting a single pathway may be compensated for by others, and that translation is limited by the absence of standardised clinical assays and validated biomarkers. The review is narrative rather than systematic and reports no new data.
Over the past 30 years, Swiss barn owls have become more reddish-brown and more heavily spotted. By analyzing the genomes of more than 3,000 birds, scientists at the University of Lausanne identified the genetic variants linked to these changes in plumage and revealed natural selection at work. Their findings, published in Nature Communications, show that evolution can happen rapidly in the wild.
In the early days of the COVID-19 pandemic, many households wiped down groceries with disinfectant before putting them away. Hand sanitizer was in short supply. With little information on how the virus spread – people became more cautious of germs from other people. A new University of California San Diego study suggests that humans may not be alone in changing behavior after experiencing a disease threat.
A new study shows that barn owls crossed the Atlantic Ocean from Europe to the Caribbean islands, where they diversified and evolved into giant forms, less than two million years ago. They've since dispersed from the Caribbean to the Galápagos and from the Caribbean to the mainland American continents.
KRAS G12C inhibitors provide an important treatment option for patients with KRAS G12C-mutant lung cancer, but some tumors respond poorly from the outset. Alterations in KEAP1, a gene involved in cellular stress responses, are associated with reduced sensitivity to these drugs.
Some KRAS G12C-mutant lung cancers are resistant to KRAS G12C inhibitors from the outset. Loss of KEAP1 increases expression of pyruvate carboxylase (PC), allowing cancer cells to maintain metabolites required for growth during treatment. Genetic deletion of PC restored sensitivity to sotorasib and enhanced tumor suppression in mouse models.