Results 101 to 110 of about 181,236 (248)
Oral squamous cell carcinoma cells exhibit upregulated expression of GSDMD upon exposure to low‐dose cisplatin chemotherapy, which subsequently interacts with MMP14 through its N‐terminal domain, activating the epithelial‒mesenchymal transition (EMT) process and promoting the lymph node metastasis of oral squamous cell carcinoma.
Zixian Huang+9 more
wiley +1 more source
Background: Osteoarthritis (OA) is a progressive, age-associated disease that is characterized with cartilage destruction, subchondral bone remodeling and inflammation of the synovial membrane.
Taherian+3 more
doaj
The C-terminal domain of 72 kDa gelatinase A is not required for catalysis, but is essential for membrane activation and modulates interactions with tissue inhibitors of metalloproteinases [PDF]
Gillian Murphy+5 more
openalex +1 more source
This study proposes a novel HCC therapy using CA‐4S2@ES‐Cu nanomedicines to amplify cuproptosis, enhancing chemotherapy and immunotherapy. CA‐4 and ES‐Cu synergistically inhibit tumor growth, induce immune responses, and reverse the immunosuppressive microenvironment, offering an effective multidimensional therapeutic strategy for HCC treatment ...
Yingjie Zeng+16 more
wiley +1 more source
This study develops enucleated MSC‐derived microvesicles (Mito@euMVs) to deliver functional mitochondria for optimizing wound repair. By efficiently encapsulating mitochondria, Mito@euMVs rejuvenate hyperglycemia‐induced senescent fibroblasts and HUVECs. Using PVA microneedle patches, the therapeutic efficacy of Mito@euMVs is validated in diabetic rats
Zixuan Dong+3 more
wiley +1 more source
The paper considers the current pathogenesis, by choosing the actual targets of pharmacotherapy with available drugs. It reflects the cytokine mechanisms responsible for lesion of the synovial membranes, cartilage, and subchondral bone.
A V Naumov
doaj
First structure of a snake venom metalloproteinase: a prototype for matrix metalloproteinases/collagenases. [PDF]
F. Xavier Gomis‐Rüth+2 more
openalex +1 more source
Aortic dissection (AD) is accompanied by a decrease in CCDC80 in vascular smooth muscle cells (VSMCs). CCDC80 can interact with JAK2, and VSMC‐specific CCDC80 deficiency accelerates the progression of AD by activating the JAK2/STAT3 pathway involved in regulating the phenotype switching and function of VSMCs.
Qingqing Xiao+18 more
wiley +1 more source