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PMID |
Sentence |
1 |
30862678
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Dual specificity phosphatases (DUSPs) are a family of phosphatases mainly responsible for MAPK inhibition.
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2 |
30862678
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Diabetes-induced DUSP4 reduction enhanced p38 and c-Jun N-terminal kinase (JNK) activity and podocyte dysfunction.
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3 |
30862678
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The overexpression of DUSP4 prevented the activation of p38, JNK, caspase 3/7 activity, and NADPH oxidase 4 expression induced by high glucose level exposure.
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4 |
30862678
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These morphological changes were associated with profound podocyte foot process effacement, cell death, and sustained p38 and JNK activation.
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5 |
30862678
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Moreover, inhibition of protein kinase C-δ prevented DUSP4 expression decline and p38/JNK activation in the podocytes and renal cortex of diabetic mice.
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6 |
31155289
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Dual-specificity phosphatase 26 (DUSP26) is a member of the Dusp protein family, and is suggested to be involved in divers biological and pathological processes, such as cell growth, differentiation, inflammation and apoptosis.
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7 |
31155289
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DUSP26 deficiency accelerated renal injury and dysfunction, as evidenced by the elevated glomerulosclerosis, reduced expression of Nephrin and promoted glomerular basement membrane thickness.
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8 |
31155289
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Moreover, STZ-induced fibrosis in kidney glomeruli of DN mice was markedly prolonged in DUSP26-knockout mice through potentiating transforming growth factor-β1 (TGF-β1) expression.
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9 |
31155289
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More importantly, reducing ROS generation could significantly abolish DUSP26 knockdown-exacerbated TGF-β1 expression and MAPKs activation, thereby protecting podocytes from GLU-induced podocyte injury.
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