Research
Transplantation Research & Renal Pathophysiology
PPP1R3G-mediated necroptosis in kidney disease
Tubular cell injury and death are key drivers of both acute and chronic kidney disease. Among the mechanisms involved, regulated cell death has emerged as a pivotal contributor to disease progression. RIPK1 (receptor-interacting protein kinase 1) is a central regulator of inflammation and cell death, with its activity tightly controlled by phosphorylation and ubiquitination. Our project focuses on elucidating how PPP1R3G (protein phosphatase 1 regulatory subunit 3G) partners with PP1γ to remove inhibitory phosphorylation from RIPK1, thereby activating its kinase function and promoting cell death. Based on these insights, we are developing peptidomimetics to selectively block PPP1R3G/PP1γ interactions, with the ultimate goal of preventing RIPK1-dependent cell death and reducing kidney disease progression.
Macula densa NOS1β and transplanted kidney graft function
Dietary bicarbonate supplementation elevates urinary pH and upregulates MDNOS1β expression in the kidney. This upregulation attenuates vasoconstriction and suppresses the tubuloglomerular feedback response, ultimately improving graft function and enhancing post-transplant renal outcomes
Reducing ischemic kidney injury through application of a synchronization modulation electric field
One of the earliest impairments in ischemia is dysfunction of the Na⁺/K⁺-ATPase (Na/K pump), caused by insufficient ATP supply, which leads to progressive cellular damage. Our lab is exploring strategies to preserve ATP and sustain Na/K pump activity as a way to reduce renal injury. We developed Synchronization Modulation Electric Field (SMEF), a novel approach designed to maintain Na⁺/K⁺-ATPase activity even under ATP-deficient conditions. Applying SMEF during cold storage of donor kidneys helps preserve ATP levels, prevent Na⁺/K⁺-ATPase translocation, and protect mitochondrial integrity—ultimately improving graft viability and function.
Kidney–Liver crosstalk
This project explores kidney–liver crosstalk, particularly the role of Metabolic Associated Steatohepatitis (MASH) in chronic kidney disease (CKD). Leveraging our expertise in rodent liver transplantation, we developed a model by transplanting livers between MASH and normal mice—either from MASH donors to healthy recipients or vice versa—to isolate and investigate the specific contribution of hepatic pathology to CKD.
Large animal models
In collaboration with the USF–TGH Transplant Research Center, our lab utilizes advanced porcine models to investigate organ graft function under clinically relevant conditions. Through procedures such as kidney and liver transplantation, ischemia–reperfusion injury, and machine perfusion, we are able to closely mimic human physiology and surgical scenarios. These large-animal models serve as a robust platform for evaluating graft viability, optimizing preservation strategies, and developing novel therapeutic interventions to improve transplant outcomes.
Funding Support
NIH-NIDDK (R01DK122050) (04/16/2020 - 03/31/2026)
Macula densa NOS1 and transplanted renal graft function
NIH-NIDDK (R01DK138092) (04/01/2024 - 03/31/2029)
Protection of donor kidney and transplanted graft function by modulating Na/K ATPase activity
NIH-NIDDK (R42DK130764)(09/16/2022 - 09/15/2025)
Protection of donor kidneys with synchronization modulation electric field (SMEF)
FHT Match Corridor MED052 (09/19/2024 - 07/31/2026)
Matching Grant Research Program tied to STTR R42DK130764
NIH-NIDDK (R01DK145695) (12/01/2025 - 11/30/2030)
Mechanisms of NASH-mediated pathogenesis of CKD ; Scored 7%, Pending council meeting)