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Anarchy in the UPR: A Ca(2+)-insensitive PKC inhibits SERCA activity to promote ER stress


Nonalcoholic fatty liver disease (NAFLD) is highly prevalent in Western countries, and is linked to the development of liver cancer and Type 2 diabetes (T2D). It is strongly associated with obesity, but the dysregulation of liver lipid storage is not fully understood. Fatty acid oversupply to hepatocytes can establish a vicious cycle involving diminished protein folding, endoplasmic reticulum (ER) stress, insulin resistance and further lipogenesis. This commentary discusses the recent findings of Lai et al. published in Bioscience Reports, that implicate protein kinase C delta (PKCdelta) activation by fatty acids in the inhibition of the SERCA Ca(2+) pump, resulting in reduced ER Ca(2+) loading and protein misfolding. PKCdelta therefore represents a target for the treatment of both steatosis and insulin resistance, key to the prevention of NAFLD and T2D.

Type Journal
ISBN 1573-4935 (Electronic) 0144-8463 (Linking)
Authors Schmitz-Peiffer, C.
Responsible Garvan Author A/Prof Carsten Schmitz-Peiffer
Published Date 2018-02-08
Published Pages pii: BSR20170966
Status Always Electronic
DOI 10.1042/BSR20170966
URL link to publisher's version
OpenAccess link to author's accepted manuscript version