- Director of Translational Medicine, Division of Nephrology
- The Herrlich Lab
Patients seen at
- Physical Address: 4921 Parkview Place, Saint Louis, MO, United States
- Mailing Address: 4921 Parkview Place
Suite C, 5th Floor
St. Louis, MO 63110
- Phone: 314-362-7603
- Fax: 314-747-2460
- Physical Address: 400 N Lindbergh Blvd, Saint Louis, MO, United States
- Mailing Address: 400 N. Lindbergh Blvd
St. Louis, MO 63141
- Phone: 314-989-0886
- Fax: 314-989-0596
- Physical Address: 4950 Childrens Place, Saint Louis, MO, United States
- Mailing Address: 4950 Children’s Place
St. Louis, MO 63110
- Phone: 314-362-7209
- Fax: 314-362-7232
Dr. Herrlich in the News:
- Andreas Herrlich Receives VA Merit Award
- Dr. Andreas Herrlich Receives 1.45M R01 Grant to Study Amphiregulin and Kidney Fibrosis
- Andreas Herrlich Heads EMBO Summer Lecture on Fibrosis
- Herrlich Awarded $1.125M Grant from NIDDK to Study ADAM17
- Nephrology Training: Brigham and Women’s Hospital/Massachusetts General Hospital
- Chief Residency: Johns Hopkins Bayview Medical Center
- Residency: Johns Hopkins Bayview Medical Center
- Medical Degree: Berlin, Germany (0)
- Medical License
- Ameican Board of Internal Medicine
- American Board of Nephrology
- Missouri Medical License
Our Lab is interested in understanding cellular and molecular mechanisms that orchestrate tissue injury, repair and fibrosis in the kidney as well as deleterious effects of kidney disease in other organs (interorgan crosstalk).
Acute kidney injury (AKI) and fibrotic chronic kidney disease (CKD) and their secondary complications, cardiovascular disease and lung injury, are highly prevalent world-wide and cause significant morbidity and mortality. Therapeutic strategies to prevent kidney injury or fibrosis and secondary organ damage are lacking.
Recently, we are particularly interested in kidney-released growth factors, cytokines and their receptors that control injury, repair and fibrosis in the kidney and that are involved in organ to organ crosstalk, such as the kidney-lung, kidney-heart or kidney-liver axis.
We are using mouse models of acute kidney injury and chronic kidney disease, combined with cardiac, lung or liver injury, as well as cell culture models. We are defining critical cell types and signaling mediators/pathways involved in tissue injury-repair, fibrosis and organ crosstalk using a combination of cell-based studies, genomic/bioinformatics analysis (shRNA, siRNA, CRISPR-Cas9, functional genomics, single cell RNAseq), novel genetically-engineered mouse models, clinical specimens, and targeted therapeutics.
Visit the Herrlich Lab.
Kefaloyianni E., Raja Keerthi Raja M., Schumacher J., Muthu ML., Krishnadoss V., Waikar SS, Herrlich A (2019) Proximal tubule-derived amphiregulin amplifies and integrates profibrotic EGFR signals in kidney fibrosis. Journal of the American Society of Nephrology, accepted, accepted August 2019.
Kefaloyianni E, Muthu LM, Kaeppler J, Sun X, Sabbisetti V, Chalaris A, Rose-John S, Wong E, Sagi I, Waikar SS, Rennke H, Humphreys BD, Bonventre JV., Herrlich A.* (2016) ADAM17 substrate release in proximal tubule drives kidney fibrosis. Journal of Clinical Investigation Insight, 18;1(13). pii: e87023; PMID: 27642633.
Parra L., Hartmann M., Schubach S., Yong L., Herrlich P.* and Herrlich A.* (2016) Growth factor and co-receptor release by structural regulation of substrate metalloprotease accessibility. Scientific Reports, 2016 Nov 23;6:37464. DOI: 10.1038/srep37464. *co-senior authors.
Hartmann, M., Parra, L. M., Ruschel, A, Lindner, C., Morrison, H., Herrlich, A.*, and Herrlich, P*. (2015) Inside-out Regulation of Ectodomain Cleavage of Cluster-of-Differentiation-44 [CD44] and of Neuregulin-1 requires Substrate Dimerization. The Journal of Biological Chemistry, PMID: 25925953. *co-senior authors.
“JBC Paper of the week” and “JBC Paper of the Year 2015” in the Signal Transduction Category
Dang M., Armbruster N., Miller M. A., Cermeno E., Hartmann M., Bell G. W., Root D. E., Lauffenburger D. A., Lodish H. F., and Herrlich A. (2013) Regulated ADAM17-dependent EGF family ligand release by substrate-selecting signaling pathways. Proceedings of the National Academy of Sciences of the United States of America, 110, 9776-9781; PMID: 23720309. Editor’s choice Science Signaling: http://stke.sciencemag.org/content/6/280/ec140