Publications
57
Citations
4,449
Est. group size
—
Recurring co-author estimate
Active years
34
Publishing since 1993
Johannes Schlöndorff studies the molecular causes of kidney disease, focusing on how genetic mutations affect specialized kidney filtering cells called podocytes and the proteins that support their structure (such as ACTN4, INF2, and TRPC6). This work aims to understand rare and genetic forms of kidney damage, including focal segmental glomerulosclerosis (FSGS) and disease linked to APOL1 gene variants, which are more common in people of African ancestry. The research combines cell biology, mouse models, and genetics to explain why certain gene mutations cause kidney injury.
Publication output has been relatively steady but modest over the last decade, with a peak in 2020 and an average of about 2 papers per year over the last 5 years.
Generated by claude-sonnet-5 from public bibliographic data · Jul 20, 2026
- Gene–disease relationships for glomerular phenotypes: expert recommendations from ClinGen
Nature Reviews Nephrology · 2026
- Differing sensitivities to angiotensin converting enzyme inhibition of kidney disease mediated by APOL1 high-risk variants G1 and G2
Kidney International · 2024
- Variant upon variant: kidney-disease risk associated with APOL1 G2 genetic variants is abrogated by the APOL1 p.N264K variant
Kidney International · 2024
- Gain-of-function, focal segmental glomerulosclerosis Trpc6 mutation minimally affects susceptibility to renal injury in several mouse models
PLoS ONE · 2022
- Trpc6 gain-of-function disease mutation enhances phosphatidylserine exposure in murine platelets
PLoS ONE · 2022
- Gain-of-function, focal segmental glomerulosclerosis <i>Trpc6</i> mutation minimally affects susceptibility to renal injury in several mouse models
bioRxiv (Cold Spring Harbor Laboratory) · 2022
- <i>Trpc6</i> gain-of-function disease mutation enhances phosphatidylserine exposure in murine platelets
bioRxiv (Cold Spring Harbor Laboratory) · 2022
- My, oh, MYO9A! Just how complex can regulation of the podocyte actin cytoskeleton get?
Kidney International · 2021
- Niacinamide May Be Associated with Improved Outcomes in COVID-19-Related Acute Kidney Injury: An Observational Study
Kidney360 · 2020
- Phosphorylation of ACTN4 Leads to Podocyte Vulnerability and Proteinuric Glomerulosclerosis
Journal of the American Society of Nephrology · 2020
- Dysregulated Dynein-Mediated Trafficking of Nephrin Causes INF2-related Podocytopathy
Journal of the American Society of Nephrology · 2020
- FSGS-Causing INF2 Mutation Impairs Cleaved INF2 N-Fragment Functions in Podocytes
Journal of the American Society of Nephrology · 2020
- Cosmc-dependent mucin-type<i>O</i>-linked glycosylation is essential for podocyte function
American Journal of Physiology-Renal Physiology · 2020
- Posaconazole-Induced Apparent Mineralocorticoid Excess
Kidney International Reports · 2020
- Increased phosphorylation of ACTN4 leads to podocyte vulnerability and proteinuric kidney disease and is stimulated by high glucose and TGF‐b
The FASEB Journal · 2020
- Kidney International×5
- Journal of the American Society of Nephrology×5
- bioRxiv (Cold Spring Harbor Laboratory)×3
- American Journal of Transplantation×2
- Kidney International Reports×2
- Edward Calomeni
Medicine · The Ohio State University
- William E. Smoyer
Medicine · The Ohio State University
- Myda Khalid
Medicine · Indiana University
- Mahmoud Kallash
Medicine · The Ohio State University
- Salem Almaani
Medicine · The Ohio State University
This profile was generated automatically from public scholarly data (OpenAlex). Group size and activity levels are estimates derived from co-authorship patterns.
Last updated Jul 19, 2026.
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