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Dr. med. Matthias J. Hackl
Department II of Internal Medicine
University Hospital Cologne
Kerpener Str. 62
50937 Cologne, Germany
+49 221 478-32319

University Hospital of Cologne
Nephrolab Cologne
CECAD Research Center
Joseph-Stelzmann-Str. 26
50931 Cologne, Germany

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Matthias Hackl

The dynamic interplay of Calcium signaling and actin remodeling in podocytes

Loss of podocytes is central to the development of focal segmental glomerulosclerosis (FSGS) and results in hypertrophy of neighboring podocytes to maintain the filtration barrier. However, the effectiveness of hypertrophy is limited and once podocyte loss exceeds the threshold of 20 %, this will result in glomerular sclerosis. For the adjustment of podocytes to hypertrophy, struggling to maintain the elaborate podocyte architecture and to prevent detachment from the basement membrane, the dynamic capacities of the actin cytoskeleton are of prime importance. Hence, in this research proposal we will address the seminal question of how the interplay of altered calcium signaling and the reorganization of the actin cytoskeleton jointly contribute to glomerular pathophysiology and to progression towards FSGS. To this end, we will employ a state-of-the-art imaging approach including intravital multiphoton microscopy, innovative reporter mouse models, serial multiphoton imaging and super-resolution technologies. The overarching goal of this research proposal is to understand the pathogenetic effect of calcium signaling and its impact on alterations of the actin cytoskeleton in podocytes.


Binz-Lotter, J., Jungst, C., Rinschen, M.M., Koehler, S., Zentis, P., Schauss, A., Schermer, B., Benzing, T., and Hackl, M.J. (2020) Injured Podocytes Are Sensitized to Angiotensin II-Induced Calcium Signaling. J Am Soc Nephrol,  31(3): 532-542.

Butt, L., Unnersjo-Jess, D., Hohne, M., Edwards, A., Binz-Lotter, J., Reilly, D., Hahnfeldt, R., Ziegler, V., Fremter, K., Rinschen, M.M., Helmstadter, M., Ebert, L.K., Castrop, H., Hackl, M.J., Walz, G., Brinkkoetter, P.T., Liebau, M.C., Tory, K., Hoyer, P.F., Beck, B.B., Brismar, H., Blom, H., Schermer, B., and Benzing, T. (2020) A molecular mechanism explaining albuminuria in kidney disease. Nat Metab,  2(5): 461-474.

Koehler, S., Brahler, S., Kuczkowski, A., Binz, J., Hackl, M.J., Hagmann, H., Hohne, M., Vogt, M.C., Wunderlich, C.M., Wunderlich, F.T., Schweda, F., Schermer, B., Benzing, T., and Brinkkoetter, P.T. (2016) Single and Transient Ca(2+) Peaks in Podocytes do not induce Changes in Glomerular Filtration and Perfusion. Sci Rep,  6: 35400.

Burford, J.L., Villanueva, K., Lam, L., Riquier-Brison, A., Hackl, M.J., Pippin, J., Shankland, S.J., and Peti-Peterdi, J. (2014) Intravital imaging of podocyte calcium in glomerular injury and disease. J Clin Invest,  124(5): 2050-8.

Hackl, M.J., Burford, J.L., Villanueva, K., Lam, L., Susztak, K., Schermer, B., Benzing, T., and Peti-Peterdi, J. (2013) Tracking the fate of glomerular epithelial cells in vivo using serial multiphoton imaging in new mouse models with fluorescent lineage tags. Nat Med,  19(12): 1661-6.