Results 191 to 200 of about 180,932 (288)
A 3D‐printed interpenetrating Ti/Zn composite enables sustained Zn2+ release to regulate intracellular Ca2+ redistribution, preserve mitochondrial homeostasis, activate ERK/MAPK signaling, and promote M2 macrophage polarization, thereby enhancing osteoimmune‐mediated bone regeneration and peri‐implant osseointegration.
Wanyi Huang +7 more
wiley +1 more source
Exercise-induced lysosomal adaptations in skeletal muscle. [PDF]
Kuznyetsova A, Hood DA.
europepmc +1 more source
FBL directly binds to and stabilizes SIRT1 by blocking its ubiquitin‐proteasome degradation, thereby sustaining nicotinamide metabolism and redox homeostasis to counteract cellular senescence in ESCC. Genetic and pharmacological suppression of FBL sensitizes tumor cells to senolytic therapy.
Xing Jin +9 more
wiley +1 more source
Mdivi-1-Sensitive Mitochondrial Remodeling Contributes to B Cell Immune Synapse Formation and Antigen Presentation. [PDF]
Bozo JP +4 more
europepmc +1 more source
GC cells enhance glutamine accumulation by upregulating SLC1A5 expression. This upregulation not only boosts GC cell proliferation, but also outcompetes CD8+ T cells for glutamine and suppresses their antitumor immunity. Mechanistically, METTL7A deficiency in GC induces SLC1A5 overexpression via an m6A‐dependent pathway and N‐glycosylation ...
Mingjun Sun +16 more
wiley +1 more source
Targeting lysosome-dependent cell death in cancer: towards therapeutic strategies. [PDF]
Li Y +6 more
europepmc +1 more source
TIPE1m NPs nanoparticles restore TIPE1 expression, promote RAB7A ubiquitination and degradation, suppress autophagic flux, and resensitize paclitaxel‐resistant triple‐negative breast cancer to therapy. ABSTRACT Acquired paclitaxel (PTX) resistance remains a major obstacle in triple‐negative breast cancer (TNBC) treatment.
Wei Hu +9 more
wiley +1 more source
Therapeutic targeting of lysosome-triggered inflammatory channels in nasal and upper-airway allergic conditions. [PDF]
Yu H +6 more
europepmc +1 more source
CuPB@HA is a CD44‐associated, plaque‐targeted nanozyme that alleviates oxidative stress, inflammation, and lipid accumulation in macrophages. By reducing CD36‐dependent lipid uptake and promoting ABCA1/ABCG1‐mediated cholesterol handling, it improves macrophage function, preferentially accumulates in atherosclerotic lesions, reduces plaque burden, and ...
Jianliang Ou +14 more
wiley +1 more source

