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. 2017 Aug 24;8:567. doi: 10.3389/fphar.2017.00567

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Copyright © 2017 Shihata, Putra and Chin-Dusting.

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) or licensor 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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The role of Caveolin-1 in cellular signaling mechanisms involved in fibrosis. Caveolin-1 (Cav-1) directly and indirectly regulates fibrotic processes in various tissues. In cardiac and lung fibrosis, Cav-1 prevents collagen deposition, fibroblast proliferation and TGFβ signaling through its negative regulation of Smad and non-Smad signaling pathways such as Rho-like GTPase, PI3K/AKT, MAPK (MEK/ERK), and JNK signaling pathways. Similarly, in kidney fibrosis, Cav-1 modulates fibrotic processes via the aforementioned pathways as well as NF-κB signaling. Of note, TGFβ signaling can also mediate Cav-1 expression via the activation of non-SMAD signaling pathways. Conversely, Cav-1 has been shown to promote kidney fibrosis by prolonging EGFR-ERK signaling. Moreover, in liver fibrosis, Cav-1 promotes liver cirrhosis through its negative regulation of eNOS (, activation; , inhibition).

Inline graphic — The role of Caveolin-1 in cellular signaling mechanisms involved in fibrosis. Caveolin-1 (Cav-1) directly and indirectly regulates fibrotic processes in various tissues. In cardiac and lung fibrosis, Cav-1 prevents collagen deposition, fibroblast proliferation and TGFβ signaling through its negative regulation of Smad and non-Smad signaling pathways such as Rho-like GTPase, PI3K/AKT, MAPK (MEK/ERK), and JNK signaling pathways. Similarly, in kidney fibrosis, Cav-1 modulates fibrotic processes via the aforementioned pathways as well as NF-κB signaling. Of note, TGFβ signaling can also mediate Cav-1 expression via the activation of non-SMAD signaling pathways. Conversely, Cav-1 has been shown to promote kidney fibrosis by prolonging EGFR-ERK signaling. Moreover, in liver fibrosis, Cav-1 promotes liver cirrhosis through its negative regulation of eNOS (, activation; , inhibition).