Results 61 to 70 of about 53,340 (302)

MicroRNA-29a Suppresses CD36 to Ameliorate High Fat Diet-Induced Steatohepatitis and Liver Fibrosis in Mice

open access: yesCells, 2019
MicroRNA-29 (miR-29) has been shown to play a critical role in reducing inflammation and fibrosis following liver injury. Non-alcoholic fatty liver disease (NAFLD) occurs when fat is deposited (steatosis) in the liver due to causes other than excessive ...
Hung-Yu Lin   +3 more
doaj   +1 more source

Treatment of growth hormone attenuates hepatic steatosis in hyperlipidemic mice via downregulation of hepatic CD36 expression

open access: yesAnimal Cells and Systems, 2020
The recombinant human growth hormone (GH) has been used for the treatment of growth hormone deficiency (GHD) and diverse short stature state, and its physiological and therapeutic effects are well documented.
Hyung Seok Jang   +5 more
doaj   +1 more source

Molecular basis of CD36 deficiency. Evidence that a 478C-->T substitution (proline90-->serine) in CD36 cDNA accounts for CD36 deficiency. [PDF]

open access: yesJournal of Clinical Investigation, 1995
CD36 deficiency is divided into two subgroups: neither platelets nor monocytes express CD36 (type I deficiency), and monocytes express CD36 in spite of the lack of platelet CD36 (type II deficiency). We have already demonstrated that a 478C-->T substitution (proline90-->serine) in platelet CD36 cDNA predominates in type II deficiency (Kashiwagi, H., S.
H, Kashiwagi   +9 more
openaire   +2 more sources

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

Metabolic Memory in Cardiovascular Disease: Encoding, Propagation, and Therapeutic Targeting

open access: yesAdvanced Science, EarlyView.
Cardiovascular risk often persists after metabolic abnormalities are corrected. This conceptual Review frames such persistence as metabolic memory, encoded through a narrowing therapeutic window from reversible marks to irreversible damage, with continuous input from peripheral organs.
Cheng Cheng   +12 more
wiley   +1 more source

Mesenchymal Stromal Cell‐Based Cell–Drug Conjugates for the Treatment of Acute Liver Failure

open access: yesAdvanced Science, EarlyView.
Mesenchymal stromal cell (MSC)‐based cell‐drug conjugates are constructed by anchoring rosiglitazone‐loaded nanoparticles onto the MSC surface. Sustained rosiglitazone release enhances MSC proliferation and paracrine activity while promoting anti‐inflammatory macrophage polarization.
Tenghui Ye   +6 more
wiley   +1 more source

CD36 and regulatory T cells

open access: yes, 2015
The effect of cluster of differentiation (CD)36 on regulatory T cells (Treg) was investigated in gonadal (GN) adipose tissues and mesenteric lymph nodes (MLN) of wild-type (WT) and CD36 deficient (CD36−/−) mice kept on standard fat (SFD, lean) or on high
Lijnen, Roger   +3 more
core   +1 more source

Deletion of CD36 exhibits limited impact on normal hematopoiesis and the leukemia microenvironment

open access: yesCellular & Molecular Biology Letters, 2023
Background CD36 has been identified as a potential therapeutic target both in leukemic cells and in the tumor immune microenvironment. In acute myeloid leukemia (AML), we found that APOC2 acts with CD36 to promote leukemia growth by activating the LYN ...
Yiting Meng   +8 more
doaj   +1 more source

The Cancer Cell Metabolic Reprogramming Remodels the Tumor Microenvironment: Molecular Mechanisms and Therapeutic Strategies

open access: yesAdvanced Science, EarlyView.
This review elucidates how cancer cell metabolic reprogramming—across glucose, lipid, amino acid, and nucleotide pathways—remodels the tumor microenvironment to suppress anti‐tumor immunity and promote immune escape. Targeting these metabolic axes offers promising strategies to overcome immunotherapy resistance and enhance cancer treatment.
Guoqing Xiang   +5 more
wiley   +1 more source

Lentiviral expression of mCherry-CD36 in CD36-/- iMOs rescues the small PV phenotype and shows the recruitment of CD36 to PVs.

open access: yes, 2016
(A) CD36-deficient iMOs exhibited smaller PVs than WT cells at 48 h of infection. The expression of mCherry-CD36 via a transducer lentiviral expression vector, restored the WT PV size to the CD36-/- iMOs.
Ricardo T. Gazzinelli (164680)   +5 more
core   +1 more source

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