Fingolimod Modulates the Gene Expression of Proteins Engaged in Inflammation and Amyloid-Beta Metabolism and Improves Exploratory and Anxiety-Like Behavior in Obese Mice

Wencel, Przemysław; Blecharz-Klin, Kamilla; Piechal, Agnieszka; Pyrzanowska, Justyna; Mirowska‐Guzel, Dagmara; Strosznajder, Robert P.

doi:10.1007/s13311-023-01403-2

Cited by 3 publications

(1 citation statement)

References 98 publications

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“…FTY720 regulates gene expression in inflammation and amyloid-β metabolism and improves exploratory and anxiety-like behaviors in obese mice. It has a positive effect on reducing inflammation-driven neurodegeneration ( 143 ). Consequently, therapies focusing on the S1P pathway can also be used to treat autoimmune diseases rather than MS. Siponimod and ozanimod have also been employed in treating recurrent MS or ulcerative colitis recently, and these drugs slow down the inflammatory progression of the disease through immunomodulatory effects ( 144 , 145 ).…”

Section: S1p Receptor Modulators In Inflammatory Diseasesmentioning

confidence: 99%

How do sphingosine-1-phosphate affect immune cells to resolve inflammation?

Sun,

Wang,

et al. 2024

Front. Immunol.

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Inflammation is an important immune response of the body. It is a physiological process of self-repair and defense against pathogens taken up by biological tissues when stimulated by damage factors such as trauma and infection. Inflammation is the main cause of high morbidity and mortality in most diseases and is the physiological basis of the disease. Targeted therapeutic strategies can achieve efficient toxicity clearance at the inflammatory site, reduce complications, and reduce mortality. Sphingosine-1-phosphate (S1P), a lipid signaling molecule, is involved in immune cell transport by binding to S1P receptors (S1PRs). It plays a key role in innate and adaptive immune responses and is closely related to inflammation. In homeostasis, lymphocytes follow an S1P concentration gradient from the tissues into circulation. One widely accepted mechanism is that during the inflammatory immune response, the S1P gradient is altered, and lymphocytes are blocked from entering the circulation and are, therefore, unable to reach the inflammatory site. However, the full mechanism of its involvement in inflammation is not fully understood. This review focuses on bacterial and viral infections, autoimmune diseases, and immunological aspects of the Sphks/S1P/S1PRs signaling pathway, highlighting their role in promoting intradial-adaptive immune interactions. How S1P signaling is regulated in inflammation and how S1P shapes immune responses through immune cells are explained in detail. We teased apart the immune cell composition of S1P signaling and the critical role of S1P pathway modulators in the host inflammatory immune system. By understanding the role of S1P in the pathogenesis of inflammatory diseases, we linked the genomic studies of S1P-targeted drugs in inflammatory diseases to provide a basis for targeted drug development.

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Section: S1p Receptor Modulators In Inflammatory Diseasesmentioning

confidence: 99%

How do sphingosine-1-phosphate affect immune cells to resolve inflammation?

Sun,

Wang,

et al. 2024

Front. Immunol.

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BACE1 inhibition via miR-6838-5p overexpression inhibits insulin resistance and the immune response in HFD-induced obesity in mice model

Han,

Quan,

Tian

et al. 2024

Immunopharmacology and Immunotoxicology

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Current View on PPAR-α and Its Relation to Neurosteroids in Alzheimer’s Disease and Other Neuropsychiatric Disorders: Promising Targets in a Therapeutic Strategy

Żulińska,

Strosznajder,

Strosznajder

2024

IJMS

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Peroxisome proliferator-activated receptors (PPARs) may play an important role in the pathomechanism/pathogenesis of Alzheimer’s disease (AD) and several other neurological/neuropsychiatric disorders. AD leads to progressive alterations in the redox state, ion homeostasis, lipids, and protein metabolism. Significant alterations in molecular processes and the functioning of several signaling pathways result in the degeneration and death of synapses and neuronal cells, leading to the most severe dementia. Peroxisome proliferator-activated receptor alpha (PPAR-α) is among the processes affected by AD; it regulates the transcription of genes related to the metabolism of cholesterol, fatty acids, other lipids and neurotransmission, mitochondria biogenesis, and function. PPAR-α is involved in the cholesterol transport to mitochondria, the substrate for neurosteroid biosynthesis. PPAR-α-coding enzymes, such as sulfotransferases, which are responsible for neurosteroid sulfation. The relation between PPAR-α and cholesterol/neurosteroids may have a significant impact on the course and progression of neurodegeneration/neuroprotection processes. Unfortunately, despite many years of intensive studies, the pathogenesis of AD is unknown and therapy for AD and other neurodegenerative diseases is symptomatic, presenting a significant goal and challenge today. This review presents recent achievements in therapeutic approaches for AD, which are targeting PPAR-α and its relation to cholesterol and neurosteroids in AD and neuropsychiatric disorders.

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Fingolimod Modulates the Gene Expression of Proteins Engaged in Inflammation and Amyloid-Beta Metabolism and Improves Exploratory and Anxiety-Like Behavior in Obese Mice

Cited by 3 publications

References 98 publications

How do sphingosine-1-phosphate affect immune cells to resolve inflammation?

How do sphingosine-1-phosphate affect immune cells to resolve inflammation?

BACE1 inhibition via miR-6838-5p overexpression inhibits insulin resistance and the immune response in HFD-induced obesity in mice model

Current View on PPAR-α and Its Relation to Neurosteroids in Alzheimer’s Disease and Other Neuropsychiatric Disorders: Promising Targets in a Therapeutic Strategy

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