PT - JOURNAL ARTICLE AU - Moruzzi, Noah AU - Valladolid-Acebes, Ismael AU - Kannabiran, Sukanya A AU - Bulgaro, Sara AU - Burtscher, Ingo AU - Leibiger, Barbara AU - Leibiger, Ingo B AU - Berggren, Per-Olof AU - Brismar, Kerstin TI - Mitochondrial impairment and intracellular reactive oxygen species alter primary cilia morphology AID - 10.26508/lsa.202201505 DP - 2022 Dec 01 TA - Life Science Alliance PG - e202201505 VI - 5 IP - 12 4099 - https://www.life-science-alliance.org/content/5/12/e202201505.short 4100 - https://www.life-science-alliance.org/content/5/12/e202201505.full SO - Life Sci. Alliance2022 Dec 01; 5 AB - 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.