Regulation of Complement Activation by Heme Oxygenase-1 (HO-1) in Kidney Injury.

Regulation of Complement Activation by Heme Oxygenase-1 (HO-1) in Kidney Injury.
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DOI:
10.3390/antiox10010060
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发表时间:
2021-01-06
期刊:
Antioxidants (Basel, Switzerland)
影响因子:
--
通讯作者:
Lianos EA
Lianos EA
中科院分区:
其他
文献类型:
--
作者:
Detsika MG;Lianos EA

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血红素加氧酶是一种细胞保护酶,具有很强的抗氧化和抗凋亡特性。其细胞保护作用主要归因于其酶活性,其涉及血红素降解为胆绿素,同时释放一氧化碳(CO)。最近的研究发现了一个新的血红素加氧酶-1(HO-1)的细胞保护作用,通过确定的补体控制蛋白衰变加速因子的调节作用。这是一种关键的补体调节蛋白,可防止可导致肾损伤的补体级联反应失调或过度活化。因此,细胞特异性靶向HO-1诱导可能是一种新的方法,以减轻补体依赖性形式的肾脏疾病。
Heme oxygenase is a cytoprotective enzyme with strong antioxidant and anti-apoptotic properties. Its cytoprotective role is mainly attributed to its enzymatic activity, which involves the degradation of heme to biliverdin with simultaneous release of carbon monoxide (CO). Recent studies uncovered a new cytoprotective role for heme oxygenase-1 (HO-1) by identifying a regulatory role on the complement control protein decay-accelerating factor. This is a key complement regulatory protein preventing dysregulation or overactivation of complement cascades that can cause kidney injury. Cell-specific targeting of HO-1 induction may, therefore, be a novel approach to attenuate complement-dependent forms of kidney disease.
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