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Targeting Peroxisome Proliferator-Activated Receptor-β/δ (PPARβ/δ) for the Treatment or Prevention of Alcoholic Liver Disease

期刊

BIOLOGICAL & PHARMACEUTICAL BULLETIN
卷 44, 期 11, 页码 1598-1606

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PHARMACEUTICAL SOC JAPAN

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alcoholic liver disease; lipid accumulation; insulin resistance; peroxisome proliferator-activated receptor (PPAR); xenobiotic-metabolizing enzyme

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Excessive and chronic alcohol consumption can lead to alcoholic liver disease, which is influenced by multiple factors and may be modulated by PPARs. PPAR beta/delta could potentially be targeted for the treatment and prevention of alcoholic liver disease, although its role requires further clarification.
Excessive, chronic alcohol consumption can lead to alcoholic liver disease. The etiology of alcoholic liver disease is multifactorial and is influenced by alterations in gene expression and changes in fatty acid metabolism, oxidative stress, and insulin resistance. These events can lead to steatosis, fibrosis, and eventually to cirrhosis and liver cancer. Many of these functions are regulated by peroxisome proliferator-activated receptors (PPARs). Thus, it is not surprising that PPARs can modulate the mechanisms that cause alcoholic liver disease. While the roles of PPAR alpha and PPAR gamma are clearer, the role of PPAR beta/delta in alcoholic liver disease requires further clarification. This review summarizes the current understanding based on recent studies that indicate that PPAR beta/delta can likely be targeted for the treatment and/or the prevention of alcoholic liver disease.

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