Results 131 to 140 of about 71,651 (313)

Targeting Regulation of Macrophage to Treat Metabolic Disease: Role of Phytochemicals

open access: yesCell Proliferation, EarlyView.
One‐third of the world's population is affected by metabolic syndrome. Complicated pathogenesis and limited drugs cause the growing prevalence of metabolic syndrome. Macrophage‐mediated metaflammation is closely associated with the development of metabolic syndrome. The role of phytochemicals targeting macrophages in the treatment of metabolic syndrome
Zeting Ye   +6 more
wiley   +1 more source

Systemic lupus erythematosus, thrombocytopenia, microangiopathic haemolytic anaemia and anti-CD36 antibodies. [PDF]

open access: bronze, 1997
Rustam Al‐Shahi Salman   +6 more
openalex   +1 more source

Repetitive Transcranial Magnetic Stimulation Induces Cognitive Recovery in Alzheimer's Disease via GABAergic Neuron Activation of the Cx3cl1‐Cx3cr1 Axis

open access: yesCell Proliferation, EarlyView.
Schematic diagram illustrating the molecular mechanisms of the Cx3cl1‐Cx3cr1 axis mediated by rTMS activation of GABAergic neurons in the process of cognitive function recovery in AD. ABSTRACT This study aimed to investigate the impact of repetitive transcranial magnetic stimulation (rTMS) on cognitive recovery in Alzheimer's disease (AD) by exploring ...
Yunxiao Kang   +7 more
wiley   +1 more source

β-Amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase [PDF]

open access: yes, 2004
β-Amyloid (βA) peptide is strongly implicated in the neurodegeneration underlying Alzheimer's disease, but the mechanisms of neurotoxicity remain controversial. This study establishes a central role for oxidative stress by the activation of NADPH oxidase
Abramov, A.Y.   +2 more
core  

Human CD36 is a high affinity receptor for the native lipoproteins HDL, LDL, and VLDL [PDF]

open access: hybrid, 1998
Dominica Calvo   +4 more
openalex   +1 more source

Mechanism of EC‐EXOs‐Derived THBS3 Targeting CD47 to Regulate BMSCs Differentiation to Ameliorate Bone Loss

open access: yesCell Proliferation, EarlyView.
EC‐EXOs could regulate the differentiation of BMSCs through the key protein THBS3, which inhibits their differentiation to lipogenic cells and promotes their differentiation to osteoblasts. THBS3 could down‐regulate the expression of its downstream target CD47 and delay the process of bone loss in aged mice and OVX mice, which may provide a novel ...
Jiaojiao Wang   +8 more
wiley   +1 more source

CD36 plays a negative role in the regulation of lipophagy in hepatocytes through an AMPK-dependent pathway[S]

open access: yesJournal of Lipid Research, 2019
Fatty acid translocase cluster of differentiation (CD36) is a multifunctional membrane protein that facilitates the uptake of long-chain fatty acids. Lipophagy is autophagic degradation of lipid droplets.
Yun Li   +10 more
doaj  

Macrophage Efferocytosis as a Therapeutic Strategy in Intervertebral Disc Degeneration

open access: yesCell Proliferation, EarlyView.
Macrophages, integral to degenerated intervertebral discs, play a critical role in disc degeneration. By performing efferocytosis, they clear apoptotic cells. This article explores the process of efferocytosis, its molecular mechanisms, potential therapeutic implications for intervertebral disc degeneration and future strategies for targeted treatments.
Shijie Chen   +9 more
wiley   +1 more source

Melanoma-Derived Extracellular Vesicles Induce CD36-Mediated Pre-Metastatic Niche

open access: yesBiomolecules
CD36 expression in both immune and non-immune cells is known to be directly involved in cancer metastasis. Extracellular vesicles (EVs) secreted by malignant melanocytes play a vital role in developing tumor-promoting microenvironments, but it is unclear
Shankar Suman   +13 more
doaj   +1 more source

Molecular Basis of CD36 Deficiency

open access: yesJapanese Journal of Thrombosis and Hemostasis, 1996
We have analyzed molecular basis of CD36 deficiency and identified three mutations responsible for CD36 deficiency: 1) a 478C→T substitution in codon 90 (proline90→serine), 2) a dinucleotide deletion in colon 110, and 3) a single nucleotide insertion in codon 317. The 478C→T (proline90→serine) substitution seemed to be the most common mutation. We have
openaire   +3 more sources

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