Mitochondrial impairment and intracellular reactive oxygen species alter primary cilia morphology

Noah Moruzzi, Ismael Valladolid-Acebes, Sukanya A. Kannabiran, Sara Bulgaro, Ingo Burtscher, Barbara Leibiger, Ingo B. Leibiger, Per Olof Berggren, Kerstin Brismar

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)
30 Downloads (Pure)


Primary cilia have recently emerged as cellular signaling organelles. Their homeostasis and function require a high amount of energy. However, how energy depletion and mitochondria impairment affect cilia have barely been addressed. We first studied the spatial relationship between a mitochondria subset in proximity to the cilium in vitro, finding similar mitochondrial activity measured as mitochondrial membrane potential compared with the cellular network. Next, using common primary cilia cell models and inhibitors of mitochondrial energy production, we found alterations in cilia number and/or length due to energy depletion and mitochondrial reactive oxygen species (ROS) overproduction. Finally, by using a mouse model of type 2 diabetes mellitus, we provided in vivo evidence that cilia morphology is impaired in diabetic nephropathy, which is characterized by ROS overproduction and impaired mitochondrial metabolism. In conclusion, we showed that energy imbalance and mitochondrial ROS affect cilia morphology and number, indicating that conditions characterized by mitochondria and radicals imbalances might lead to ciliary impairment.

Original languageEnglish
Number of pages13
JournalLife science alliance
Issue number12
Early online date14 Sept 2022
Publication statusPublished (in print/issue) - 1 Dec 2022

Bibliographical note

Funding Information:
This work was supported by Family Erling-Persson Foundation, Medical Research Council D0284901, Funds of Karolinska Institutet.

Publisher Copyright:
© 2022 Moruzzi et al.


  • Cilia/metabolism
  • Diabetes Mellitus, Type 2
  • Homeostasis
  • Humans
  • Mitochondria/metabolism
  • Reactive Oxygen Species/metabolism


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