
Figure 1: The pathophysiology of DN
The pathophysiology of DN involves several mechanisms, as hyperglycemia caused by diabetes triggers various harmful processes within the kidneys. These processes can be generally categorized into hemodynamic, metabolic, inflammatory, and oxidative stress, which are the primary contributors to the disease's development. This added glucose burden, along with increased oxidative stress, triggers a detrimental cascade that leads to tubular fibrosis and the development of DN. Abbreviations: VEGF, Vascular Endothelial Growth Factor; TGF-B, Transforming Growth Factor Beta; IGF-1, Insulin-like Growth Factor-1; RAAS, Renin-Angiotensin-Aldosterone System; PG, Prostaglandins; SGLT2, Sodium/Glucose Cotransporter 2; GFR, Glomerular Filtration Rate; TNF-a, Tumor Necrosis Factor alpha; SAA, serum amyloid A; IL-1B, Interleukin-1 beta; ROS, Reactive Oxygen Species; NOX, NADPH Oxidase; AGEs, advanced glycation end products; JAK-STAT, Janus kinase/ Signal Transducers and Activators of Transcription; MCP-1, monocyte chemoattractant protein 1; MAPK, mitogen-activated protein kinase; SMAD 2/3, suppressor of mothers against decapentaplegic 2/3; NF-kB, nuclear factor kappa B; ECM, extracellular matrix.
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