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. 2022 Sep 22;16:982074. doi: 10.3389/fncel.2022.982074

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Copyright © 2022 Wurz, Schulz, O’Bryant, Sharp and Hughes.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Cofilin-actin rod forming pathways with activators and inhibitors. Cofilin-actin rods can be induced through multiple separate pathways. Calcineurin (PP2B) or RanBP9 stimulation of SSH1 or chronophin (CIN) dephosphorylates and activates cofilin, which under stress can form aberrant rods with actin. Inhibitors of SSH1, such as 14-3-3 and pS3 peptide, can prevent rod formation. Miuraenamide and profilin overexpression can prevent actin from associating with cofilin, and tetracycline can disrupt rods. Aβ induction of integrin/RanBP9 or NOX with PrPc promotes rod formation, but Vas2870 can inhibit NOX generation of ROS. CuB activates the Gα13/RhoA/VASP pathway and increases actin assembly. LIMK, activated by PAK and RhoA/ROCK, phosphorylates and inactivates cofilin. Inhibitors of LIMK, such as the S3 peptide or Pyr-1, can promote cofilin-actin rod formation. Created with www.biorender.com.