Actin reorganization and junctional remodeling in podocyte foot process effacement

Actin dynamics during podocyte foot process effacement show distinct, origin-independent patterns in Lifeact.mScarlet-I–labeled podocytes, with slit diaphragm protein remodeling that is reversible during nephrotoxic serum nephritis.

• Why it matters: Podocyte injury drives kidney disease, but the initiating and coordinating processes behind actin-driven foot process effacement and junctional remodeling remain unclear.
• What they did: In nephrotoxic serum nephritis and other podocyte disease models, podocytes expressing Lifeact.mScarlet-I were imaged with STED microscopy to track actin patterns, while slit diaphragm composition was monitored for reversibility.
• The result: ZO-1 and Claudin-5 appeared at the plasma membrane with proteinuria onset, and both actin and junctional assembly reversed as foot process effacement resolved, proteinuria declined, and podocytes recovered.

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