Nicotine Induces Podocyte Apoptosis through Increasing Oxidative Stress

Area of Science:

• Nephrology
• Cell Biology
• Toxicology

Background:

• Cigarette smoking accelerates chronic kidney disease (CKD).
• Nicotine, a key smoking component, increases renal mesangial cell proliferation.
• This study investigates nicotine's impact on podocyte injury.

Purpose of the Study:

• To examine the effect of nicotine on podocyte apoptosis.
• To elucidate the molecular mechanisms underlying nicotine-induced podocyte injury.
• To investigate the role of nicotinic acetylcholine receptors (nAChRs) in these processes.

Main Methods:

• Assessed nAChR expression in human podocytes and mouse kidneys.
• Evaluated nicotine's effects on podocyte nephrin expression, ROS generation, proliferation, and apoptosis.
• Analyzed downstream signaling pathways (MAPKs) and utilized nAChR antagonists and inhibitors.

Main Results:

• Nicotine decreased nephrin expression and increased ROS generation and apoptosis in podocytes.
• Nicotine activated ERK1/2, JNK, and p38 signaling pathways.
• nAChR antagonists and MAPK inhibitors attenuated nicotine-induced podocyte apoptosis.

Conclusions:

• Nicotine induces podocyte apoptosis via ROS generation and MAPKs signaling.
• This mechanism contributes to smoking-associated CKD progression.
• Findings offer insights into the molecular basis of smoking-related kidney damage.