GRKs and β-Arrestins: “Gatekeepers” of Mitochondrial Function in the Failing Heart

We demonstrated that GRK2 localizes into mitochondria of macrophagic cells in a timedependent manner and an early translocation supports the cell to better respond to LPS dependent mitochondrial dysfunction

Daniela Sorriento; Jessica Gambardella; Antonella Fiordelisi; Guido Iaccarino; Maddalena Illario


Scholarcy highlights

  • Specialty section: This article was submitted to Experimental Pharmacology and Drug Discovery, a section of the journal Frontiers in Pharmacology
  • Mitochondrial function is regulated by several proteins, including GRK2 and β-arrestins which act in a G Protein-CoupledReceptor independent manner to orchestrate intracellular signaling associated with key mitochondrial processes
  • This study shows that the cAMP/PKA pathway is responsible for faster mitochondrial reactive oxygen species production, whereas β-arrestin1 signaling is responsible for the slower one
  • Several reports support the proof of concept that GRK2 and β-arrestins are able to regulate intracellular signaling in a GPCR independent manner
  • We tried to reconcile these opposing findings pointing to a protective role of GRK2 in mitochondria through its binding to heat shock protein 90
  • The available ones strongly suggest the involvement of β-arrestins in the regulation of mitochondrial ROS production and mitochondrial respiration
  • The better understanding of the role of these proteins in mitochondria could have important implications providing the basis for new therapeutic approaches to treat mitochondrial dysfunction in cardiovascular diseases

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