Results 241 to 250 of about 1,879,389 (356)

A Cold Stress‐Activated Endocrine Sentinel Chemical Hormone Promotes Insect Survival via Mitochondrial Adaptations Through the Adipokinetic Hormone Receptor

open access: yesAdvanced Science, EarlyView.
Seasonal cold adaptation is vital for insect survival, yet the molecular mechanisms linking diapause to mitochondrial resilience remain largely unresolved. We identify ascaroside C9 (asc‐C9) as a key endocrine signal that enhances diapause survival during cold stress by activating the AKHR–PGC1α–UCP4 axis, thereby driving cold‐induced lipolysis and ...
Jiao Zhou   +14 more
wiley   +1 more source

NAD⁺ Reduction in Glutamatergic Neurons Induces Lipid Catabolism and Neuroinflammation in the Brain via SARM1

open access: yesAdvanced Science, EarlyView.
NAD⁺ homeostasis maintains neuronal integrity through opposing actions of NMNAT2 and SARM1. Loss of NMNAT2 in glutamatergic neurons reprograms cortical metabolism from glucose to lipid catabolism, depletes lipid stores, and triggers inflammation and neurodegeneration.
Zhen‐Xian Niou   +9 more
wiley   +1 more source

7. Diabetes Technology: Standards of Care in Diabetes-2026. [PDF]

open access: yesDiabetes Care
American Diabetes Association Professional Practice Committee for Diabetes* .
europepmc   +1 more source

TMEM131‐Mediated Soluble TRAIL Triggered Type II Alveolar Epithelial Cell Senescence in Radiation‐Induced Lung Injury

open access: yesAdvanced Science, EarlyView.
TMEM131 recruits the COPII complex to accelerate TRAIL transportation from endoplasmic reticulum to Golgi apparatus, and promotes soluble TRAIL secretion. TRAIL inhibits mitophagy and induces senescence through DR5 receptor in type II alveolar epithelial cells, ultimately driving radiation‐induced lung injury (RILI) progression.
Linzhi Han   +10 more
wiley   +1 more source

Gut Peptide Alterations in Type 2 Diabetes and Obesity: A Narrative Review. [PDF]

open access: yesCurr Obes Rep
Tzeravini E   +4 more
europepmc   +1 more source

Lactylation‐Driven YTHDC1 Alleviates MASLD by Suppressing PTPN22‐Mediated Dephosphorylation of NLRP3

open access: yesAdvanced Science, EarlyView.
In MASLD, YTHDC1 undergoes increased lactylation and ubiquitination, reducing its expression. AARS1 mediates lactylation at lysine 565, while disrupted binding to LDHA further promotes lactylation, suppressing YTHDC1. This downregulation enhances PTPN22 mRNA stability, leading to NLRP3 dephosphorylation and activation, which exacerbates inflammation ...
Feng Zhang   +16 more
wiley   +1 more source

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