Results 201 to 210 of about 176,030 (314)

TBC1D1 functions as a negative regulator of satellite cells for muscle regeneration. [PDF]

open access: yesNat Commun
Yang X   +8 more
europepmc   +1 more source

Natural Resistance to Ovarian Hyperstimulation Syndrome in Estrildid Finches Reveals Macrophage GPR183 as a Potential Therapeutic Target

open access: yesAdvanced Science, EarlyView.
Ovarian macrophage depletion reverses OHSS resistance in estrildid finches and exacerbates OHSS symptoms in rats. Activating macrophage GPR183 alleviates OHSS by reducing pro‐inflammatory factors, increasing immunomodulatory molecules, remodeling CD44/SDC4‐mediated communication, and restoring immune homeostasis.
Xiaofei Yan   +11 more
wiley   +1 more source

“Membrane‐Guided” Repair Strategy: Precision Delivery of GGT1 Degrader for Targeted Repair and Regeneration of Spinal Cord Neurons

open access: yesAdvanced Science, EarlyView.
This study confirms that GGT1 is a key driver of neuronal ferroptosis following spinal cord injury. We developed NSCm@EA, a biomimetic delivery system coated with neural stem cell membranes, for precise delivery of enocyanin to injured neurons. By combining targeted delivery with ubiquitination degradation mechanisms, this system promotes MGRN1 ...
Tao Yang   +14 more
wiley   +1 more source

GSDME-IL-18 pyroptotic axis prevents myosteatosis by expanding tissue-resident macrophages to promote muscle regeneration. [PDF]

open access: yesJ Clin Invest
Cao Q   +15 more
europepmc   +1 more source

CK2α Deficiency Drives Myocardial Fibrosis via Desmin‐Induced Mitochondrial Dysfunction

open access: yesAdvanced Science, EarlyView.
CK2α preserves mitochondrial homeostasis by phosphorylating Desmin to recruit Cryab, ensuring proper filament assembly. CK2α deficiency disrupts this interaction, causing mitochondrial dysfunction, metabolic shifts, bioenergetic failure, and oxidative stress—ultimately establishing a pro‐fibrotic environment that drives cardiac fibrosis.
Canjie Ma   +12 more
wiley   +1 more source

Brown Adipocyte Sheets Alleviate Myocardial Ischemia–Reperfusion Injury Through NRG4–ErbB4–Dependent Ferroptosis Inhibition

open access: yesAdvanced Science, EarlyView.
Brown adipocyte sheets are engineered to protect the heart against myocardial ischemia–reperfusion injury by restraining ferroptosis. Upon transplantation onto the cardiac surface, they improve cardiac function, limit infarction and fibrosis, and enhance angiogenesis.
Lifu Sun   +6 more
wiley   +1 more source

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