Results 101 to 110 of about 10,976,092 (296)

Plaque‐Hepatic Targeting Nanotherapy Disrupts the PCSK9‐LOX‐1 Axis to Suppress oxLDL in Atherosclerosis

open access: yesAdvanced Science, EarlyView.
Self‑amplifying PCSK9–LOX‑1 feedback axis drives atherosclerotic progression by promoting oxLDL generation and endothelial uptake. A dual‑targeting nanoplatform (siPCSK9@PEAL NPs‑aL) is constructed to simultaneously silence hepatic PCSK9 for lipid lowering and block plaque LOX‑1 for anti‑inflammation.
Yi Duan   +7 more
wiley   +1 more source

A Multidimensional Engineering Strategy Reprograms Microglia via Targeted and Sustained‐Release Extracellular Vesicles for Spinal Cord Injury Repair

open access: yesAdvanced Science, EarlyView.
A multifunctional EV‐based nanoplatform (Ang‐TEVs@Gel) was engineered via preconditioning, surface targeting, and ROS‐responsive hydrogel encapsulation to reprogram microglia. This system restored autophagy via miR‐664a‐3p/PIK3CA axis, cleared myelin debris, resolved neuroinflammation, and promoted axon remyelination, ultimately achieving robust motor ...
Wu Xiong   +17 more
wiley   +1 more source

Definition of the immunogenic forms of modified human LDL recognized by human autoantibodies and by rabbit hyperimmune antibodies

open access: yesJournal of Lipid Research, 2004
Humans and laboratory animals recognize human modified LDL as immunogenic. Immune complexes (ICs) isolated from human sera contain malondialdehyde-modified LDL (MDA-LDL) and N ε(carboxymethyl)lysine-modified LDL (CML-LDL) as well as antibodies reacting ...
Gabriel Virella   +6 more
doaj   +1 more source

A Role of the Bile Salt Receptor FXR in Atherosclerosis [PDF]

open access: yes, 2010
This study reviews current insights into the role of bile salts and bile salt receptors on the progression and regression of atherosclerosis. Bile salts have emerged as important modifiers of lipid and energy metabolism.
Albert K. Groen   +12 more
core   +1 more source

Controllable Cascade Aggregation Ion Programmed Nanomachines and Simple Isolation Enable Tumor‐Derived Small Extracellular Vesicles Detection for Enhanced Breast Cancer Assessment

open access: yesAdvanced Science, EarlyView.
This study developed a convenient, enzyme‐free detection platform based on controllable aggregation ion nanomachines. Its favorable anti‐interference capacity and high sensitivity meet the detection requirements for clinical samples processed via a simple filtration method within 10 min.
Zhihao Zhang   +8 more
wiley   +1 more source

Association of Ad36 with Low Density Lipoprotein.

open access: yes, 2012
Association of Ad36 with Low Density Lipoprotein.
Takashi Kadowaki (35402)   +2 more
core   +1 more source

SR‐A3 Promotes USP18‐Mediated deISGylation of STING to Protect Against Myocardial Ischemia‐Reperfusion Injury

open access: yesAdvanced Science, EarlyView.
MI/RI is a major clinical challenge with high morbidity and mortality. This study demonstrates that SR‐A3 expression is downregulated in MI/RI, and its deletion exacerbates damage via the USP18/ISG15/STING axis, revealing SR‐A3 as a potential therapeutic target.
Yufei Han   +24 more
wiley   +1 more source

Thematic review series: Patient-Oriented Research. What we have learned about VLDL and LDL metabolism from human kinetics studies

open access: yesJournal of Lipid Research, 2006
Lipoprotein metabolism is the result of a complex network of many individual components. Abnormal lipoprotein concentrations can result from changes in the production, conversion, or catabolism of lipoprotein particles. Studies in hypolipoproteinemia and
Klaus G. Parhofer, P. Hugh R. Barrett
doaj   +1 more source

Flow diagram of the analysis strategy (Abbreviations: WC, waist circumference; TG, triglyceride; HDL, high-density-lipoprotein; LDL, low-density-lipoprotein).

open access: yes, 2015
Flow diagram of the analysis strategy (Abbreviations: WC, waist circumference; TG, triglyceride; HDL, high-density-lipoprotein; LDL, low-density-lipoprotein).
Jeanette Bahr (775942)   +5 more
core   +1 more source

SPARC Drives Podocyte Mitochondrial Damage and Ferroptosis in Diabetic Kidney Disease Following Klotho Deficiency

open access: yesAdvanced Science, EarlyView.
Klotho deficiency promotes podocyte mitochondrial dysfunction and ferroptosis through activation of the PKCα/CUX1/SPARC/TGFβ‐RII axis. SPARC emerges as a key mediator linking Klotho loss to podocyte injury in DKD and other kidney injury models, suggesting broader implications for CKD progression.
Qing Yang   +11 more
wiley   +1 more source

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