Calcium Signaling As a Therapeutic Target for Liver Steatosis

Eunüs S. Ali, Nikolai Petrovsky

Research output: Contribution to journalReview articlepeer-review

33 Scopus citations


Hepatic steatosis, the first step in nonalcoholic fatty liver disease (NAFLD), can arise from various pathophysiological conditions. While lipid metabolism in the liver is normally balanced such that there is no excessive lipid accumulation, when this homeostasis is disrupted lipid droplets (LDs) accumulate in hepatocytes resulting in cellular toxicity. The mechanisms underlying this accumulation and the subsequent hepatocellular damage are multifactorial and poorly understood, with the result that there are no currently approved treatments for NAFLD. Impaired calcium signaling has recently been identified as a cause of increased endoplasmic reticulum (ER) stress contributing to hepatic lipid accumulation. This review highlights new findings on the role of impaired Ca 2+ signaling in the development of steatosis and discusses potential new approaches to NAFLD treatment based on these new insights.

Original languageEnglish
Pages (from-to)270-281
Number of pages12
JournalTrends in Endocrinology and Metabolism
Issue number4
StatePublished - Apr 2019

Bibliographical note

Publisher Copyright:
© 2019 Elsevier Ltd


  • NASH
  • PKC
  • calcium signaling
  • fatty liver
  • steatohepatitis
  • type 2 diabetes

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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