Kidney aging and regeneration

Research Group Leader

  • Prof. Dr. med. Roland Schmitt 


Research Assistants

  • Dr. rer. nat. Inga Sörensen-Zender 
  • Dr. med. Vera Wulfmeyer 
  • Dr. med. Nikolai Rex
  • Blanca de Juan, PhD student
  • Cand. med. Julius Sinnig, MD student
  • Cand. med. Nils Funk, MD student
  • Cand. med. Johanna Jost, MD student


Technical Assistants

  • Britta Gewecke 
  • Michaela Beese 


Scientific profile

In acute kidney injury, tubular cells normally respond with a well-coordinated sequence of epithelial repair and regeneration designed to restore organ structure and function. Under certain circumstances, such as aging or pre-existing chronic damage, these processes are defective or insufficient, resulting in maladaptation, atrophy and fibrosis. Our focus is to explore novel pathomechanisms underlying these defective processes. We focus on renal candidate molecules and signaling pathways that are regulated in an age-dependent manner.  In particular, we are interested in the cross-talk of epithelial cells and inflammatory cells and in cell cycle regulation processes. In old age and chronic diseases, there is an accumulation of senescent cells in the kidney, which are in a permanent cell cycle arrest and damage the kidney by secreting bioactive molecules (senescence-associated secretory phenotype). In recent years, it has been shown that antagonizing or eliminating senescent cells, can protect the kidney and other organs and improve impaired repair processes.  

Ultimately, our studies should provide a basis on which new therapeutic strategies can be developed to improve the repair and regeneration potential of old or pre-damaged kidneys. In this way, we hope to halt the progression of chronic renal insufficiency and enable people with kidney disease to achieve better health. 


Selected publications

Gaedcke S, Sinning J, Dittrich-Breiholz O, Haller H, Soerensen-Zender I, Liao CM, Nordlohne A, Sen P, von Vietinghoff S, DeLuca DS, Schmitt R. Single-Cell versus Single-Nucleus: Transcriptome differences in murine kidney after ischemia-reperfusion injury. Am J Physiol Renal Physiol. 2022 May 30. doi: 10.1152/ajprenal.00453.2021. Epub ahead of print. PMID: 35635323. 


Liao CM, Wulfmeyer VC, Chen R, Erlangga Z, Sinning J, von Mässenhausen A, Sörensen-Zender I, Beer K, von Vietinghoff S, Haller H, Linkermann A, Melk A, Schmitt R. Induction of ferroptosis selectively eliminates senescent tubular cells. Am J Transplant. 2022 May 23. doi: 10.1111/ajt.17102. Epub ahead of print. PMID: 35607817. 


Sörensen-Zender I, Rong S, Haller H, Schmitt R. The Therapeutic Potential of Zinc-Alpha2-Glycoprotein (AZGP1) in Fibrotic Kidney Disease. Int J Mol Sci. 2022 Jan 7;23(2):646. 


Liao CM, Wulfmeyer VC, Swallow M, Falk CS, Haller H, Korstanje R, Melk A, Schmitt R. Induction of Stress-Induced Renal Cellular Senescence In Vitro: Impact of Mouse Strain Genetic Diversity. Cells. 2021 Jun 8;10(6):1437. 


Huscher D, Ebert N, Soerensen-Zender I, Mielke N, Schaeffner E, Schmitt R. Development of a prediction model for mortality and cardiovascular outcomes in older adults taking into account AZGP1. Sci Rep. 2021 Jun 3;11(1):11792. 


Haddad G, Kölling M, Wegmann UA, Dettling A, Seeger H, Schmitt R, Soerensen-Zender I, Haller H, Kistler AD, Dueck A, Engelhardt S, Thum T, Mueller TF, Wüthrich RP, Lorenzen JM. Renal AAV2-Mediated Overexpression of Long Non-Coding RNA H19 Attenuates Ischemic Acute Kidney Injury Through Sponging of microRNA-30a-5p. J Am Soc Nephrol. 2021 Feb;32(2):323-341. 


Sen P, Helmke A, Liao CM, Sörensen-Zender I, Rong S, Bräsen JH, Melk A, Haller H, von Vietinghoff S, Schmitt R. SerpinB2 Regulates Immune Response in Kidney Injury and Aging. J Am Soc Nephrol. 2020 May;31(5):983-995. 


Wulfmeyer VC, Auber B, Haller H, Schmitt R. Comparison of Different Selection Strategies for Tolvaptan Eligibility among Autosomal Dominant Polycystic Kidney Disease Patients. Am J Nephrol. 2019;50(4):281-290. 


Sörensen-Zender I, Chen R, Rong S, David S, Melk A, Haller H, Schmitt R. Binding to carboxypeptidase M mediates protective effects of fibrinopeptide Bβ15-42. Transl Res. 2019 Nov;213:124-135. 


Schmitt R, Melk A. Molecular mechanisms of renal aging. Kidney Int. 2017 Sep;92(3):569-579. 


Current third-party funding

Die pathophysiologische Bedeutung des Zellzyklus im akuten Nierenversagen 

Sponsor: Deutsche Forschungsgemeinschaft 

PI: SCHM 2146/11-1, 2022-2025 


Senolyse bei Nierenerkrankung: Therapeutisches Potential und Risiken 

Sponsor: Deutsche Forschungsgemeinschaft 

PI: SCHM 2146/10-1, 2020-2024 


Open positions and PhD projects

We are looking for motivated team members with high interest in biomedical research. Our open projects are mainly related to issues of cellular and molecular senotherapy and epithelial and inflammatory cell responses in renal repair. Depending on the applicant profile, project objectives will be adapted for medical student or PhD theses, which may be offered within the structured programs (HBRS-Molecular Medicine; StrucMed) or independently. For medical students, usually at least one semester of dedicated time should be scheduled in the lab.  If interested, please send a CV and a letter of motivation to schmitt.roland(at)  



E-Mail schmitt.roland(at)