Results 171 to 180 of about 2,514,304 (294)

Mitochondria‐Targeted Multimodal Nanotherapeutics Suppress Oxidized mtDNA‐Driven Inflammation at the Source

open access: yesAdvanced Science, EarlyView.
Ox‐mtDNA fragments escaping from mitochondria drive robust inflammatory responses. A targeted nanoplatform simultaneously inhibits mitochondrial FEN1‐mediated mtDNA cleavage and scavenges ROS, preventing the generation of immunogenic Ox‐mtDNA fragments. The released SeNPs further promote autophagic clearance of cytosolic mtDNA. Consequently, cGAS‐STING,
Wen‐Ling Li   +7 more
wiley   +1 more source

Editorial: Rodent-borne diseases: “One Health” perspectives

open access: yesFrontiers in Veterinary Science
Veasna Duong   +4 more
doaj   +1 more source

TH/TRs–COL11A2 Axis Mediates Loss of a Differentiated Astrocyte State in Hypogyrified Brains

open access: yesAdvanced Science, EarlyView.
Using a gyrencephalic congenital hypothyroidism pig model, this study reveals cerebral atrophy and cortical hypogyrification. Single‐cell sequencing identifies astrocytes as major TH‐responsive cells, with the COL11A2‐enriched Astro‐2 state nearly absent.
Ying Zhang   +14 more
wiley   +1 more source

Glucocorticoid Receptor Signaling in Myeloid Cells Orchestrates Inflammation Resolution and Muscle Repair

open access: yesAdvanced Science, EarlyView.
Glucocorticoids (GC) are widely used to reduce inflammation. We show that the glucocorticoid receptor in myeloid cells regulates macrophage cell cycle and genome integrity during muscle regeneration. We demonstrate that dexamethasone administration during the early inflammatory phase delays muscle repair by increasing macrophage proliferation ...
Sirine Souali‐Crespo   +11 more
wiley   +1 more source

CRISPR and Gene Augmentation Rescue Trabecular Meshwork Dysfunction in iPSC Models of Lowe Syndrome

open access: yesAdvanced Science, EarlyView.
By modeling Lowe syndrome using patient‐derived iPSCs, this study establishes a human disease model that faithfully recapitulates OCRL deficiency‐associated ciliary and cytoskeletal defects. The model enables evaluation of both mutation‐agnostic DNA augmentation and CRISPR‐mediated mutation correction strategies, both of which restore OCRL function and
Siyu Chen   +11 more
wiley   +1 more source

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