Results 151 to 160 of about 63,253 (224)

Development of MDM2‐Targeting PROTAC for Advancing Bone Regeneration

open access: yesAdvanced Science, EarlyView.
This work presents a creative pipeline for developing MDM2‐targeting PROTACs (MDM2‐PROTACs) for application in bone regeneration. The developed PROTACs (CL144 and CL174) are validated for their degradation efficiency and osteogenic effects in human BMSCs.
Sol Jeong   +17 more
wiley   +1 more source

Targeted Delivery of α‐ketoglutarate to Macrophages in Bone: A Novel Therapeutic Strategy for Improving Fracture Healing in Type 2 Diabetes

open access: yesAdvanced Science, EarlyView.
The study reveals that glutaminolysis in macrophages is inhibited under type 2 diabetes mellitus (T2DM) conditions, which impedes fracture healing by reducing bone morphogenetic protein 2 (BMP2) production through increased cytosine methylation on the promoter.
Jing Wang   +12 more
wiley   +1 more source

IR783‐Stabilized Nanodrugs Enhance Anticancer Immune Response by Synergizing Oxidation Therapy and Epigenetic Modulation

open access: yesAdvanced Science, EarlyView.
IR783‐stabilized nanodrugs composed of NIR dye IR783, ROS inducer β‐lapachone, and epigenetic modulator CUDC101 are designed for breast cancer immunotherapy. The nanodrugs can not only promote cancer cell apoptosis through HDAC inhibition‐enhanced oxidation therapy but also reshape the immunosuppressive microenvironment, which provides a novel strategy
Jinzhao Liu   +6 more
wiley   +1 more source

A Novel Theranostic Strategy for Malignant Pulmonary Nodules by Targeted CECAM6 with 89Zr/131I‐Labeled Tinurilimab

open access: yesAdvanced Science, EarlyView.
This study investigates the integrated diagnostic and therapeutic strategy utilizing 89Zr/131I‐labeled tinurilimab for the management of malignant lung nodules, with a particular focus on lung adenocarcinoma (LUAD). CEACAM6, which is highly expressed in most LUAD patients, activates the Src/FAK signaling pathway, thereby promoting cell proliferation ...
Chongyang Chen   +8 more
wiley   +1 more source

Asprosin‐FABP5 Interaction Modulates Mitochondrial Fatty Acid Oxidation through PPARα Contributing to MASLD Development

open access: yesAdvanced Science, EarlyView.
Aided by FABP5, abnormally elevated asprosin in hepatocytes enters the nucleus, targets and inhibits PPARα binding to the CPT1A promoter, thereby suppressing FAO. Circulating asprosin exacerbates insulin resistance, collectively driving MASLD progression.
Yuan‐Yuan Yu   +13 more
wiley   +1 more source

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