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Multiple synergistic anti-aging effects of vascular cell adhesion molecule 1 functionalized nanoplatform to improve age-related neurodegenerative diseases.
J Control Release
January 2025
School of Medicine, Chongqing University, 131 Yubei Street, Shapingba District, Chongqing 400044, China. Electronic address:
Aging is a critical factor in the onset and progression of neurodegenerative diseases and cognitive decline, with aging-related neuroinflammation and cellular senescence being major contributors. In the aging brain, the cerebral vascular endothelium overexpresses vascular cell adhesion molecule 1 (VCAM1), activating microglia and leading to neuroinflammation and cognitive impairment. Quercetin, a natural neuroprotective agent widely used for treating neurodegenerative diseases, their therapeutic efficacy, however, is limited by its poor water solubility and inability to penetrate the blood-brain barrier (BBB).
View Article and Find Full Text PDFSophaline B inhibits non-small cell lung cancer by activating NLRP3/caspase-1/GSDMD-dependent pyroptosis and PI3K/AKT/mTOR-mediated autophagy.
Nat Prod Res
January 2025
Institute of Biopharmaceutical and Health Engineering, State Key Laboratory of Chemical Oncogenomics, Shenzhen Key Laboratory of Gene and Antibody Therapy, Shenzhen International Graduate School, Tsinghua University, Shenzhen, Guangdong, China.
Sophaline B (SPB), extracted from the seeds of L., is a natural bioactive compound that effectively exerts antiviral activities against the hepatitis B virus. This is the first study to demonstrate that SPB exerts anti-tumor effects on NSCLC by inducing pyroptosis and autophagy.
View Article and Find Full Text PDFIrbesartan May Ameliorate Ventricular Remodeling by Inhibiting CREB-Mediated Cardiac Aldosterone Synthesis in Rats with Myocardial Infarction.
Int J Mol Sci
December 2024
Department of Cardiology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510800, China.
Irbesartan improves ventricular remodeling (VR) following myocardial infarction (MI). This study investigates whether irbesartan attenuates VR by reducing aldosterone production in the heart and its underlying mechanisms. MI was induced in male Sprague-Dawley rats through coronary artery ligation.
View Article and Find Full Text PDFSupramolecular Engineering of Nanoceria for Management and Amelioration of Age-Related Macular Degeneration via the Two-Level Blocking of Oxidative Stress and Inflammation.
Adv Sci (Weinh)
January 2025
Eye Center, The Second Affiliated Hospital, School of Medicine, Zhejiang Provincial Key Laboratory of Ophthalmology, Zhejiang Provincial Clinical Research Center for Eye Diseases, Zhejiang Provincial Engineering Institute on Eye Diseases, Zhejiang University, 88 Jiefang Road, Hangzhou, 310009, China.
Age-related macular degeneration (AMD), characterized by choroidal neovascularization (CNV), is the global leading cause of irreversible blindness. Current first-line therapeutics, vascular endothelial growth factor (VEGF) antagonists, often yield incomplete and suboptimal vision improvement, necessitating the exploration of novel and efficacious therapeutic approaches. Herein, a supramolecular engineering strategy to construct moringin (MOR) loaded α-cyclodextrin (α-CD) coated nanoceria (M@CCNP) is constructed, where the hydroxy and newly formed carbonyl groups of α-CD interact with the nanoceria surface via O─Ce conjunction and the isothiocyanate group of MOR inserts deeply into the α-CD cavity via host-guest interaction.
View Article and Find Full Text PDFAnti-Syndecan 2 Antibody Treatment Reduces Edema Formation and Inflammation of Murine Laser-Induced CNV.
Transl Vis Sci Technol
January 2025
Yale Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.
Purpose: Alteration of visual acuity in wet age-related macular degeneration (AMD) is mostly driven by vascular endothelial growth factor A (VEGF-A)-induced edema from leaky newly forming blood vessels below the retina layers. To date, all therapies aimed at alleviation of this process have relied on inhibition of VEGF-A activity. Although effective in preventing vascular leak and edema, this approach also leads to the loss of normal vasculature and multiple related side effects.
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