Angiotensin Converting Enzyme‐2 Therapy Improves Liver Fibrosis and Glycemic Control in Diabetic Mice With Fatty Liver

Indu G. Rajapaksha, Lakmie S. Gunarathne, Khashayar Asadi, Ross Laybutt, Sof Andrikopoulous, Ian E. Alexander, Mathew J. Watt, Peter W. Angus, Chandana B. Herath – 22 December 2021 – Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease and is frequently associated with type 2 diabetes. However, there is no specific medical therapy to treat this condition. Angiotensin‐converting enzyme 2 (ACE2) of the protective renin angiotensin system generates the antifibrotic peptide angiotensin‐(1‐7) from profibrotic angiotensin II peptide.

Redundant Functions of ERK1 and ERK2 Maintain Mouse Liver Homeostasis Through Down‐Regulation of Bile Acid Synthesis

Francesca Cingolani, Yunshan Liu, Yang Shen, Jing Wen, Alton B. Farris, Mark J. Czaja – 21 December 2021 – Activation of extracellular signal–regulated kinase (ERK) 1/2 promotes hepatocyte proliferation in response to growth stimuli, but whether constitutive hepatocyte ERK1/2 signaling functions in liver physiology is unknown. To examine the role of ERK1/2 in hepatic homeostasis, the effects of a knockout of Erk1 and/or Erk2 in mouse liver were examined. The livers of mice with a global Erk1 knockout or a tamoxifen‐inducible, hepatocyte‐specific Erk2 knockout were normal.

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