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Nicotine, smoking, podocytes, and diabetic nephropathy
Edgar A Jaimes1, Ming-Sheng Zhou2, Mohammed Siddiqui3
1Renal Service, Memorial Sloan Kettering Cancer Center, New York, New York.
American Journal of Physiology. Renal Physiology
|January 18, 2021
Summary
Nicotine in cigarettes and e-cigarettes contributes to diabetic nephropathy progression by damaging kidney podocytes. This study shows nicotine harms kidney function, independent of other smoking chemicals.
Area of Science:
- Nephrology
- Toxicology
- Cell Biology
Background:
- Diabetic nephropathy (DN) is a leading cause of end-stage kidney disease.
- Cigarette smoking (CS) and electronic cigarettes (ECs) worsen DN, but the role of nicotine (NIC) is unclear.
- Podocyte injury is a key driver of DN progression.
Purpose of the Study:
- To investigate the direct role of nicotine in diabetic nephropathy progression.
- To determine the molecular mechanisms by which nicotine affects podocytes.
Main Methods:
- Experiments were conducted using human podocytes and a mouse model of diabetic nephropathy.
- Nicotine's effects on podocyte molecular pathways, including NADPH oxidase, cyclooxygenase-2, AMP-activated protein kinase, and CD36, were analyzed.
- Proteinuria, synaptopodin, and fibronectin expression were measured in diabetic mice exposed to nicotine.
Main Results:
- Nicotine activated NADPH oxidase in podocytes, initiating a cascade involving cyclooxygenase-2, downregulation of AMP-activated protein kinase, and upregulation of CD36.
- Nicotine exposure led to increased lipid uptake and apoptosis in podocytes.
- In diabetic mice, nicotine increased proteinuria, decreased synaptopodin, and increased fibronectin expression.
Conclusions:
- Nicotine itself, independent of other smoking components, contributes to diabetic nephropathy progression.
- Nicotine-induced podocyte injury is a significant factor in the adverse effects of CS and ECs on kidney health.
- Targeting nicotine's effects may offer a new strategy to mitigate kidney damage in diabetic smokers.
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