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PKC isoforms are activated by hyperglycaemia. This editorial elegantly describes the specific PKC isoforms possibly involved in diabetes-induced organ damage. Using PKC-isoform-specific knock-out mice, the specific role of individual PKD isoforms such as PKC
and ß was identified. The mechanism of the development of albuminuria following high glucose activation of PKC isoforms is mediated via three different molecular mechanisms. PKC isoform specificity and cellular diversity seem to be responsible for the divergent outcome leading to albuminuria and/or fibrosis.
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