Prof. Ganesh PATHARE

Assistant Professor
BVSc, PhD
Office Address
Room 2-507, Block 2, 5/F, To Yuen Building31, To Yuen Street, City University of Hong Kong
Office Tel
+852 3442-6782
Email
gpathare@cityu.edu.hk
Biography URL
CityUHK Scholars

Prof. Ganesh Pathare is a veterinarian-scientist with a research focus on the bone–kidney axis and kidney diseases. He is currently an Assistant Professor in the Department of Infectious Diseases and Public Health at City University of Hong Kong. He earned his BVSc degree from Nagpur Veterinary College, India, and completed a PhD in Physiology at the University of Tuebingen, Germany, in 2014. Following a brief research position at Radboud University in the Netherlands, he completed Marie Curie Postdoctoral Fellowship at the University of Bern, Switzerland. He later taught Veterinary Physiology at St. George’s University, Grenada. Most recently, he served as a Senior Lecturer in the Medical and subsequently the Veterinary Faculty at the University of Zurich, where he also led an independent research group.

Prof. Pathare’s training and academic positions span multiple continents, shaping both his research and teaching perspectives. He has a strong interest in teaching anatomy and physiology to veterinary students. Moreover, he has authored over 25 original research articles in leading journals, including Kidney International, Journal of the American Society of Nephrology, Journal of Biological Chemistry, and American Journal of Physiology – Renal Physiology.

Preprints:

  1. Salas-Bastos A#., Bardet C#., Kopper K., Jauze L., Collaud F., Francois A., Chen G., Mohammadi M., Stockmann C., Sommer L., Loffing J., Ronzitti G*., Pathare G*. Gene therapy targeting sustained FGF23-ERK signaling alleviates kidney inflammation. (#*equal contribution). bioRxiv. https://doi.org/10.1101/2024.01.18.576116
  1. Moor M.B., Kopper K., Pechère-Bertschi A., Sagmeister M.S., Hardy R.S., Feraille E., Fuster D.G., Loffing J., Pathare G. High-salt diet modulates endocrine regulation between cortisol and FGF23. bioRxiv. https://doi.org/10.1101/2025.08.14.670453

Selected best 10 publications

  1. Bourqui L., Trnjanin A., Kopper K., Loffing-Cueni D., Radvanyi Z., Karpovich A., Rahimi T., Santos R., Wengi A., Pastor J., Moe O., Loffing J*., Pathare G*. Klotho in the kidney distal convolution regulates urinary Klotho excretion and kidney calcium reabsorption, but not phosphate homeostasis. (*equal contribution). Kidney Int. 2026 Jan. https://doi.org/10.1016/j.kint.2026.01.030

  2. Radvanyi Z, Yoo EJ, Kandasamy P, Salas-Bastos A, Monnerat S, Refardt J, Christ-Crain M, Hayashi H, Kondo Y, Jantsch J, Rubio-Aliaga I, Sommer L, Wagner CA, Hediger MA, Kwon HM, Loffing J, Pathare G. Extracellular sodium regulates fibroblast growth factor 23 (FGF23) formation. J Biol Chem. 2023 Nov. https://doi.org/10.1016/j.jbc.2023.105480.

  3. Pathare G, Dhayat NA, Mohebbi N, Wagner CA, Bobulescu IA, Moe OW, Fuster DG. Changes in V-ATPase subunits of human urinary exosomes reflect the renal response to acute acid/alkali loading and the defects in distal renal tubular acidosis. Kidney Int. 2018 Apr. https://doi.org/10.1016/j.kint.2017.10.018.

  4. Pathare G#, Anderegg M, Albano G, Lang F, Fuster DG. Elevated FGF23 Levels in Mice Lacking the Thiazide-Sensitive NaCl cotransporter (NCC). Sci Rep. 2018 Feb. (#Correspondence). https://doi.org/10.1038/s41598-018-22041-1.

  5. Pathare G, Tutakhel OAZ, van der Wel MC, Shelton LM, Deinum J, Lenders JWM, Hoenderop JGJ, Bindels RJM. Hydrochlorothiazide treatment increases the abundance of the NaCl cotransporter in urinary extracellular vesicles of essential hypertensive patients. Am J Physiol Renal Physiol. 2017 Jun. https://doi.org/10.1152/ajprenal.00644.2016.

  6. Fakhri H*, Pathare G*, Fajol A, Zhang B, Bock T, Kandolf R, Schleicher E, Biber J, Föller M, Lang UE, Lang F. Regulation of mineral metabolism by lithium. Pflugers Arch. 2014 Mar doi: https://doi.org/10.1007/s00424-013-1340-y. (*shared first author).

  7. Pathare G, Föller M, Michael D, Walker B, Hierlmeier M, Mannheim JG, Pichler BJ, Lang F. Enhanced FGF23 serum concentrations and phosphaturia in gene targeted mice expressing WNK-resistant SPAK. Kidney Blood Press Res. 2012 Dec. https://doi.org/10.1159/000343393.

  8. Pathare G, Föller M, Daryadel A, Mutig K, Bogatikov E, Fajol A, Almilaji A, Michael D, Stange G, Voelkl J, Wagner CA, Bachmann S, Lang F. OSR1-sensitive renal tubular phosphate reabsorption. Kidney Blood Press Res. 2012 Apr. https://doi.org/10.1159/000343405.

  9. Tang C, Pathare G, Michael D, Fajol A, Eichenmüller M, Lang F. Downregulation of Klotho expression by dehydration. Am J Physiol Renal Physiol. 2011 Oct. https://doi.org/10.1152/ajprenal.00037.2011.

  10. Föller M, Kempe DS, Boini KM, Pathare G, Siraskar B, Capuano P, Alesutan I, Sopjani M, Stange G, Mohebbi N, Bhandaru M, Ackermann TF, Judenhofer MS, Pichler BJ, Biber J, Wagner CA, Lang F. PKB/SGK-resistant GSK3 enhances phosphaturia and calciuria. J Am Soc Nephrol. 2011 May. https://doi.org/10.1681/asn.2010070757.

Bone-Kidney Axis and Regeneration 

Our lab investigates the bone–kidney axis and its role in kidney disease. We are also interested in harnessing this axis for regeneration to restore kidney function and mineral balance.

The vertebrate endoskeleton not only supports locomotion but also regulates mineral and energy metabolism through constant cross-talk with the kidneys. The co-evolution of this axis enabled the development of calcium–phosphate-based skeletons, a crucial adaptation for terrestrial life. Central to this axis is the bone-derived hormone fibroblast growth factor 23 (FGF23) and its co-receptor Klotho, expressed in the kidney. Together, the FGF23–Klotho pathway regulates phosphate and vitamin D metabolism. Dysregulation of this pathway is now recognized as a potential driver of chronic kidney disease (CKD), which affects ~10% of humans and >40% of aging cats, making it a critical area of both human and veterinary health.

Our research focuses on how disturbances in the FGF23–Klotho axis contribute to CKD progression and aging-like phenotypes, and on identifying strategies for therapeutic intervention.

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Fig.: Fig.: The FGF23–Klotho axis in mineral metabolism and CKD. FGF23 regulates phosphate and calcium balance by acting on the kidney through FGF receptors in the presence of Klotho. Dysregulation contributes to CKD–mineral bone disorder (CKD-MBD) and aging-related changes.

We apply a multidisciplinary approach, combining genetically engineered mouse models, advanced in vitro assays, transcriptomics, single-nucleus RNA sequencing, human cohorts, and analyses of human urinary exosomes.

Ongoing Projects:

  1. Investigating mechanisms regulating FGF23 formation and its influence on bone remodelling.

  2. Defining the segment-specific roles of Klotho in the renal tubules in health and CKD.

  3. Developing therapeutic strategies to suppress FGF23-mediated ill effects in CKD and restore kidney function.

  4. Exploring the role of the FGF23–Klotho axis in aging-like phenotypes and its relevance to human aging.

The long-term goal of our research is to translate mechanistic insights from the bone–kidney axis into novel therapeutic strategies for CKD and age-related mineral disorders. These efforts aim to benefit both human and animal health, advancing the One Health initiative.