Septin 7 mediates high glucose-induced podocyte apoptosis

Area of Science:

• Nephrology
• Cell Biology
• Molecular Medicine

Background:

• Podocyte depletion is a key feature of diabetic nephropathy (DN).
• Hyperglycemia-induced podocyte apoptosis contributes to podocyte depletion in DN.
• The precise mechanisms of hyperglycemia-induced podocyte apoptosis are not fully understood.

Purpose of the Study:

• To investigate the role of septin 7 in hyperglycemia-induced podocyte apoptosis.
• To evaluate septin 7 expression in DN and its effect on podocyte apoptosis in vitro.

Main Methods:

• Assessed septin 7 expression in human and mouse DN podocytes.
• Examined the effect of high glucose (HG) on cultured podocyte apoptosis.
• Utilized siRNA to knockdown septin 7 expression.
• Measured intracellular calcium (Ca2+) concentrations.

Main Results:

• Septin 7 expression was significantly elevated in glomerular podocytes of DN patients and db/db mice.
• HG stimulation increased septin 7 expression in cultured podocytes.
• Knockdown of septin 7 attenuated HG-induced podocyte apoptosis.
• Reducing septin 7 also decreased excessive intracellular Ca2+ concentration.

Conclusions:

• Septin 7 expression is upregulated in diabetic nephropathy.
• Septin 7 promotes podocyte apoptosis under high glucose conditions.
• Septin 7 represents a potential therapeutic target for preventing podocyte loss in DN.