Results 311 to 320 of about 5,397,691 (379)

DNA‐PKcs‐Driven YAP1 Phosphorylation and Nuclear Translocation: a Key Regulator of Ferroptosis in Hyperglycemia‐Induced Cardiac Dysfunction in Type 1 Diabetes

open access: yesAdvanced Science, EarlyView.
In the context of chronic hyperglycemia, a DDR is initiated, leading to the pathological activation of DNA‐PKcs in the diabetic heart. This activated DNA‐PKcs directly interacts with and phosphorylates YAP1 at Thr226, thereby increasing the nuclear expression of YAP1.
Junyan Wang   +10 more
wiley   +1 more source

Accurate Delivery of Mesenchymal Stem Cell Spheroids With Platelet‐Rich Fibrin Shield: Enhancing Survival and Repair Functions of Sp‐MSCs in Diabetic Wound Healing

open access: yesAdvanced Science, EarlyView.
Autologous plasma‐derived platelet‐rich fibrin (PRF) is prepared as a protective shield for mesenchymal stem cell spheroids (Sp‐MSCs). PRF forms a fibrin shield to protect Sp‐MSCs from the oxidative stress environment. The nutrients in PRF, particularly the α‐granules, can enhance the repair function of Sp‐MSCs.
Jinglve Zhang   +10 more
wiley   +1 more source

Genetics‐Based Targeting Strategies for Precise Neuromodulation

open access: yesAdvanced Science, EarlyView.
In this Review, the fundamental principles and implementation protocols of genetics‐based precision neuromodulation are first introduced. Then, wireless and low‐invasive strategies based on nano‐transducing materials are highlighted, along with a dissection and analysis of the strengths and weaknesses of representative studies.
Yuyuan He   +11 more
wiley   +1 more source

Collagen-Povidone Injection as Treatment for Stenosing Tenosynovitis in Older Adults With Type 2 Diabetes Mellitus. [PDF]

open access: yesPlast Reconstr Surg Glob Open
Segura-Castillo JL   +13 more
europepmc   +1 more source

Neuraminidase 1 Exacerbated Glycolytic Dysregulation and Cardiotoxicity by Destabilizing SIRT1 through Interactions with NRF2 and HIF1α

open access: yesAdvanced Science, EarlyView.
NEU1, a key regulator of glycolysis, is markedly upregulated following DOX treatment. This upregulation is attributed to HIF1α’s transcriptional repression, requiring intricate interactions with NRF2. Increased NEU1 facilitates SIRT1 lysosomal degradation, contributing to aberrant glycolytic phenotype and cardiac damage.
Ting Gao   +13 more
wiley   +1 more source

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