Results 171 to 180 of about 174,460 (337)
sEVs have a critical role in orchestrating interorgan crosstalk and mediating exercise‐induced therapeutic effects. Lin et al. demonstrates that sEVs miR‐17/20a‐5p mediates the muscle‐brain crosstalk and emphasizes the central role of mTOR signaling in executing molecular programs that can protect brain health in response to exercise. Abstract Physical
Huawei Lin+21 more
wiley +1 more source
A CMTM6 Nanobody Overcomes EGFR‐TKI Resistance in Non‐Small Cell Lung Cancer
Overcoming EGFR‐TKI resistance remains a critical challenge in NSCLC treatment. This study identifies CMTM6 as a key regulator of EGFR stability and demonstrates that a novel anti‐CMTM6 nanobody disrupts the CMTM6‐EGFR interaction. Targeting CMTM6 restores EGFR degradation, suppresses tumor growth, and confers therapeutic benefit in both CDX and PDX ...
Lu Xia+18 more
wiley +1 more source
Schematic diagram showing the potential mechanism of bigelovin on the activation of NLRP3 inflammasome Bigelovin may inhibit activated protein C kinase 1 (RACK1) by directly binding with cys168 of RACK1. Bigelovin thus prevents oligomerization of NLRP3 (NLRP3 active conformation) and subsequent assembly of NLRP3 inflammasome, blocking the activation of
Jian Cui+17 more
wiley +1 more source
Lysosome Stabilization by Leukocyte Granule Membrane Antiserum [PDF]
Robert H. Persellin
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CTSK plays a critical role in pulmonary fibrosis. Excessive CTSK accumulation interacts with SNX9 to enhance TGF‐β1‐induced SMAD3 activation and GLS1 expression in fibroblasts, driving glutamine metabolism for collagen biosynthesis and exacerbating pulmonary fibrosis.
Mengting Chen+10 more
wiley +1 more source
Lysosomes, chromosomes and cancer [PDF]
A. C. Allison, Gillian R. Paton
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Apoptotic Bodies Restore NAD and Mitochondrial Homeostasis in Fibroblasts
Mesenchymal stem cell‐derived apoptotic bodies (MSC‐ABs) target keloid fibroblasts (KFs), restoring nicotinamide adenine dinucleotide (NAD) metabolism and mitochondrial function, suppressing collagen overproduction, and rebalancing tissue homeostasis, offering a novel therapy for keloid.
Shutong Qian+10 more
wiley +1 more source
Autophagy in liver diseases: A matter of what to remove and whether to keep [PDF]
Yin, Xiao-Ming
core +1 more source
In vivo SALI therapy is achieved by scavenging intracellular ROS levels, downregulating inflammatory factors expression levels, inducing macrophage M2 directional polarization, and activating Keap1/Nrf‐2/HO‐1 pathway to reprogram redox homeostasis, induce cellular autophagy, reduce systemic inflammation, and promote liver tissue repair. Abstract Sepsis
Tao Qin+21 more
wiley +1 more source
This work designs an in situ proliferating peptide nanoparticle as a flexible resolution that modulates the neuro‐glia unit to enable enhanced multi‐target combinational therapy for secondary brain damage following subarachnoid hemorrhage. Abstract Subarachnoid hemorrhage (SAH), a lethal stroke subtype, involves complex pathological cascades triggered ...
Yibin Zhang+8 more
wiley +1 more source