Molecular insights into chronic glomerulonephritis and dopamine interplay

Abstract

|Glomerulonephritis (GN) is a rare kidney disorder associated with prolonged inflammation, fibrosis, and mitochondrial dysfunction at the glomeruli layer and nearby capillaries, which leads to the loss of glomeruli integrity and function. A pathogen-driven immune response is most often responsible for acute glomerulonephritis (AGN). In contrast, chronic glomerulonephritis (CGN) is more severe and characterized by irreversible loss of glomerular integrity with excessive fibrosis, often leading to progression to end-stage renal disease. Few pathways, such as WNT, Notch, PI3K/AKT, JAK-STAT, Complement, cGAS-STING, and TGF-β, have been linked to the progression and development of glomerular injury, characterized by mitochondrial dysfunction, inflammation, and fibrosis. However, the AMPK pathway has been reported to be protective against glomerular deterioration. Additionally, the dopaminergic system in the kidney has been linked to protecting glomerular integrity by downregulating mitochondrial dysfunction, inflammation, and fibrosis. This review highlights pathways that can potentially deteriorate and protect glomerular health. Additionally, it also provides an overview of the role of the dopaminergic system in attenuating glomerular injury. Suchdiscussion will provide a comprehensive understanding of potential therapeutic targets for attenuating CGN.

Keywords: AMPK; Chronic glomerulonephritis; Chronic kidney disease; Dopamine; Fibrosis; Mitochondrial dysfunction.