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The laboratory of Rannar Airik, PhD focuses on identifying the genetic and molecular mechanisms of chronic kidney disease including renal ciliopathies that may be targetable by therapy. To achieve this, the lab combines transgenic animal models and biochemical assays that provide a basis for further molecular dissection of the mechanisms involved in these human diseases.
Chronic kidney disease is a devastating condition that affects an increasing number of people in the world. It leads to a progressive loss of kidney function in affected individuals and ultimately necessitates dialysis or kidney transplantation for survival. The Airik Lab has demonstrated that impairment of DNA damage response in the kidney tubular epithelium can lead to kidney tubular injury and precipitate progressive fibrotic changes in the kidney, culminating in loss of kidney function. Investigating the role of DNA damage response in normal tubular maintenance and assessing how its deficiency underpins chronic kidney pathology is a high priority of our work.
MCM6 gene expression (orange) in karyomegalic tubular cells.
Renal ciliopathies are a group of fibrocystic kidney diseases that are caused by structural or functional defects in the primary cilium, a whip-like cell-surface organelle, that regulates the activity of several cellular signaling pathways. Accordingly, mutations in ciliary genes, such as those encoding nephrocystins and nephronophthisis (NPHP) proteins, compromise the cilium and result in fibrocystic kidney pathology. Although, being a major genetic cause of childhood end-stage kidney disease, the pathomechanisms underlying NPHP are not well understood. To get better insights into the disease mechanisms and to develop therapies against this condition, we use transgenic animal models and cell culture systems.
Principal Investigator rannar.airik@chp.edu Read More>>
Merlin Airik, PhD Post-doctoral Fellow
Amy B. Huynh Research Technician
The Airik Lab UPMC Children’s Hospital of Pittsburgh John G. Rangos Sr. Research Center 4401 Penn Avenue Pittsburgh, PA 15224 412-692-6229
Primary coenzyme Q10 nephropathy, a potentially treatable form of steroid-resistant nephrotic syndrome Tan W, Airik R Pediatric Nephrology 2021 Jan 22
Roscovitine Blocks Collecting Duct Cyst Growth in Cep164-deficient Kidneys Airik R, Airik M, Schueler M, Bates CM, Hildebrandt F Kidney International 2019 Aug
Delayed Onset of Smooth Muscle Cell Differentiation Leads to Hydroureter Formation in Mice with Conditional Loss of the Zinc Finger Transcription Factor Gene Gata2 in the Ureteric Mesenchyme Weiss AC, Bohnenpoll T, Kurz J, Blank P, Airik R, Lüdtke TH, Kleppa MJ, Deuper L, Kaiser M, Mamo TM, Costa R, von Hahn T, Trowe MO, Kispert A The Journal of Pathology 2019 Mar 27
Treatment with 2,4-Dihydroxybenzoic Acid Prevents FSGS Progression and Renal Fibrosis in Podocyte-Specific Coq6 Knockout Mice Widmeier E, Airik M, Hugo H, Schapiro D, Wedel J, Ghosh CC, Nakayama M, Schneider R, Awad AM, Nag A, Cho J, Schueler M, Clarke CF, Airik R, Hildebrandt F Journal of the American Society of Nephrology 2019 Feb 8
Osteoclast Stimulation Factor 1 (Ostf1) KNOCKOUT Increases Trabecular Bone Mass in Mice Vermeren M, Lyraki R, Wani S, Airik R, Albagha O, Mort R, Hildebrandt F, Hurd T Mammalian Genome 2017 Dec
SDCCAG8 Interacts with RAB Effector Proteins RABEP2 and ERC1 and Is Required for Hedgehog Signaling Airik R, Schueler M, Airik M, Cho J, Ulanowicz KA, Porath JD, Hurd TW, Bekker-Jensen S, Schrøder JM, Andersen JS, Hildebrandt F PLoS One 2016 May 25
The Airik Lab is always welcoming applications from enthusiastic students or post-docs looking to work with us. For more information, please contact Dr. Airik via email.
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