NU 2022-202
INVENTORS
Pinelopi Kapitsinou*
Ratnakar Tiwari
SHORT DESCRIPTION
Inhibition of MCT4 slows the progression of acute kidney inury to chronic kidney disease
BACKGROUND
Acute kidney inury (AKI) is a sudden onset of kidney dysfunction, often caused by factors such as ischemia, toxins, or infections, leading to impaired filtration and accumulation of waste products in the blood. If not adequately managed, AKI can progress to chronic kidney disease (CKD) and contribute to long-term kidney damage. A critical complication of AKI is fibrosis, a process where excessive connective tissue develops in the kidneys, leading to scarring and permanent damage; this fibrosis can hinder the kidney’s ability to repair itself. Novel therapeutic strategies are needed to prevent the transition from AKI to CKD.
ABSTRACT
Northwestern researchers have developed a therapy for AKI which targets the monocarboxylate transporter 4 (MCT4), a lactate transporter upregulated under hypoxic conditions. Researchers induce ischemic acute kidney injury in wild type mice and administer the MCT4 inhibitor syrosingopine. Following treatment with the MCT4 inhibitor, kidneys in the treated group are visually better perfused, demonstrate a 62% reduction in fibrosis histologically, and show significant reduction in levels of prefibrotic inflammatory genes. Taken together, these results indicate a potential novel therapeutic for AKI that can be successfully administered following injury, preventing the transition to chronic kidney disease.
APPLICATIONS
ADVANTAGES
Inhibits long-term disease progression to chronic kidney disease
Various targeting mechanisms including inhibiting, suppressing, or genetic targeting
IP STATUS
US patent application filed
Kidneys treated with MCT4 inhibitor have increased levels of blood perfusion and decreased levels of fibrotic tissue.