Two Duke Department of Medicine faculty members are among the 2025 researchers elected to the American Society for Clinical Investigation (ASCI), one of the nation’s oldest medical honor societies. ASCI supports the scientific efforts, educational needs, and clinical aspirations of physician-scientists to improve health.
Elected to the society are physician-scientists Opeyemi A. Olabisi, MD, PhD, and Tomokazu Souma, MD, PhD, both associate professors in the Division of Nephrology.
Dr. Opeyemi Olabisi
Dr. Olabisi’s research goal is to discover and characterize the mechanisms of APOL1-mediated kidney disease (AMKD), the most common form of genetic kidney disease in African Americans, for the purpose of innovative prevention and cure.
As a postdoctoral fellow, he identified APOL1-mediated cation transport as the upstream trigger of cytotoxicity. Since starting his independent lab, his research group has shown that APOL1-cation transport depolarizes plasma membrane triggering a cascade of signaling events including novel activation of GPCR-IP3-calcium signaling, reduction of mitochondrial ATP production, reduction of amino acid import and global protein synthesis. His research identified and validated APOL1 pore function as a therapeutic target for AMKD.
Recognizing the importance of community engagement to translational research, Dr. Olabisi’s lab leads a robust community engagement effort that offers African Americans free screening for AMKD, which also enabled his lab to develop a unique human iPSC-based model of AMKD. He is the principal investigator of an NIH-funded, phase 2 clinical trial of a Jak inhibitor, which blocks APOL1 synthesis.
Dr. Tomokazu Souma
Tomokazu Souma, MD, PhD, is an investigator at the Duke Regeneration Center. The central focus of his research is to understand the molecular pathways of renal repair after acute kidney injury (AKI) at single-cell resolution with the goal of identifying pathways that can facilitate renal repair and regeneration to prevent the future development of chronic kidney disease (CKD) and improve cardiovascular outcomes.
His lab made fundamental discoveries in ferroptosis, an iron-dependent, lipid-peroxidation-driven, regulated cell death modality, and he established a new paradigm that ferroptosis is not a simple all-or-none response to injury but that compasses dynamic cell state alterations, ranging from reprogramming of cell state and loss of cell plasticity to death.
Further, Dr. Souma showed the first evidence that ferroptosis is a sex-dependent driver of maladaptive repair after AKI. His research collectively pinpoints the significant possibility of leveraging endogenous female resilience factors against ferroptosis to improve renal repair after injury in both sexes during AKI in order to prevent the transition to CKD.
His group is currently working on molecular mechanisms by which ferroptosis survivors promote chronic inflammation and fibrosis through intercellular communications with renal macrophages, as well as mechanisms that govern impaired cellular plasticity in these cells in a sex-dependent manner. He is also active in collaboration to advance clinically impactful studies in related areas, such as transplantation-induced kidney damage, ferroptosis in failed repair in other organs, and interrogation of human kidneys at single-cell resolution.