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12/15-脂加氧酶与糖尿病微血管并发症

摘要

Recently,some scholars found that overexpression and activation of 12/15-lipoxygenase may contribute to the progress of diabetic nephropathy and neuropathy.12/15-1ipoxygenase can catalyze arachidonic acid to produce 12( S)- and 15 ( S)- hydroxyeicosatetraenoic acids,which may affect cell structure,metabolism and signal transduction.Some studies showed that 12/15-lipoxygenase and its metabolites can directly induce and indirectly regulate cytokines,leading to cell hypertrophy,proliferation and extracellular matrix deposition,which participate in the development of diabetic nephropathy.Moreover,overexpression and activation of 12/15-lipoxygenase could be related to oxidative and nitrative stress of the peripheral nervous system,which is probably involved in the onset of diabetic neuropathy.Therefore,12/15-lipoxygenase inhibitors and 12/15-lipoxygenase inhibitor-containing combination therapies may provide a new research direction for diabetic microvascular complications.%最近研究发现,12/15-脂加氧酶的过表达或激活可能促进了糖尿病肾病和神经病变的进展.该酶可催化花生四烯酸产生12-羟基二十碳四烯酸和15-羟基二十碳四烯酸,从而影响细胞结构、代谢和信号转导.研究发现12/15-脂加氧酶及其代谢产物可直接诱导或间接调节细胞因子导致细胞肥大、增殖和细胞外基质堆积,参与糖尿病肾病的发生.此外,该酶的过表达和激活与外周神经系统的氧化-硝化应激相关,可能参与糖尿病神经病变的发生.因此,12/15-脂加氧酶抑制剂或包含抑制剂的联合治疗可能为糖尿病微血管并发症的治疗提供新的研究方向.

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