Hydrogen peroxide-inducible clone 5 (Hic-5) as a potential therapeutic target for vascular and other disorders

Joo-ri Kim-Kaneyama, Kim-Kaneyama JR, Xiao-Feng Lei, Lei XF, Shigeko Arita, Arita S, Miyauchi A, Aya Miyauchi, Miyazaki T, Takuro Miyazaki, Miyazaki A, Akira Miyazaki
Journal of atherosclerosis and thrombosis · 2012 · doi:10.5551/jat.10736 · PMID:22472216
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-07-16 ⓘ

Hic-5 knockout mice exhibit delayed arterial media recovery after injury due to increased smooth muscle cell apoptosis, suggesting Hic-5 is a novel factor in vascular remodeling and a potential therapeutic target for various fibrotic and cancerous disorders.

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This paper is a review describing hydrogen peroxide-inducible clone-5 (Hic-5), a focal adhesion scaffold protein primarily expressed in vascular and visceral smooth muscle cells, and summarizing evidence from prior work and other pathophysiological contexts. It notes that mice lacking Hic-5 appear normal overall, but arterial media recovery after vascular injury is delayed, linked to increased apoptosis of cultured vascular smooth muscle cells after mechanical stress; the gene is also induced by transforming growth factor-β, which is associated with fibrosis. The review further discusses proposed roles for Hic-5 in fibrotic disorders and reports that siRNA silencing of Hic-5 in a breast cancer cell line reduces invasiveness, while also stating it functions as a steroid hormone co-activator and likely participates in endometriosis (among other cancers), with the caveat that evidence is compiled across conditions rather than presented as new experimental results in this article. Relevance to endometriosis: the paper explicitly states that Hic-5, as a steroid hormone co-activator, likely participates in endometriosis, though its main focus is positioning Hic-5 as a therapeutic target across vascular and multiple disorders.

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Abstract

Hydrogen peroxide-inducible clone-5 (Hic-5) is a focal adhesion scaffold protein primarily expressed in vascular and visceral smooth muscle cells. We recently generated mice lacking Hic-5, which grew with no apparent abnormality (Kim-Kaneyama J, et al. J Mol Cell Cardiol. 2011;50(1):77-86). However, we discovered that recovery of arterial media following vascular injury is delayed significantly in Hic-5 knockout mice consequent to enhanced apoptosis of cultured vascular smooth muscle cells after mechanical stress; thus, Hic-5 is regarded as a novel factor in vascular remodeling. The Hic-5 gene is also induced by transforming growth factor-β, a well-known accelerator in fibrosis. Hic-5 involvement in various fibrotic disorders, e.g., scar formation, keloid formation and glomerulosclerosis, has been proposed. siRNA silencing of Hic-5 in a breast cancer cell line reduces its invasiveness; moreover, Hic-5 serves as a steroid hormone co-activator and likely participates in endometriosis and prostate cancer. Thus, functional characterization of Hic-5 in various pathophysiological conditions may afford novel mechanistic insights into a wide variety of diseases.
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Review Hydrogen Peroxide-Inducible Clone 5 (Hic-5) as a Potential Therapeutic Target for Vascular and Other Disorders 2012 Volume 19 Issue 7 Pages 601-607 Details Abstract Hydrogen peroxide-inducible clone-5 (Hic-5) is a focal adhesion scaffold protein primarily expressed in vascular and visceral smooth muscle cells. We recently generated mice lacking Hic-5, which grew with no apparent abnormality (Kim-Kaneyama J, et al. J Mol Cell Cardiol. 2011;50(1):77-86). However, we discovered that recovery of arterial media following vascular injury is delayed significantly in Hic-5 knockout mice consequent to enhanced apoptosis of cultured vascular smooth muscle cells after mechanical stress; thus, Hic-5 is regarded as a novel factor in vascular remodeling. The Hic-5 gene is also induced by transforming growth factor-β, a well-known accelerator in fibrosis. Hic-5 involvement in various fibrotic disorders, e.g., scar formation, keloid formation and glomerulosclerosis, has been proposed. siRNA silencing of Hic-5 in a breast cancer cell line reduces its invasiveness; moreover, Hic-5 serves as a steroid hormone co-activator and likely participates in endometriosis and prostate cancer. Thus, functional characterization of Hic-5 in various pathophysiological conditions may afford novel mechanistic insights into a wide variety of diseases. この記事はクリエイティブ・コモンズ [表示 - 非営利 - 継承 4.0 国際]ライセンスの下に提供されています。 https://creativecommons.org/licenses/by-nc-sa/4.0/deed.ja Favorites & Alerts Recently viewed articles Predecessor

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endometriosis

MeSH descriptors

Antineoplastic Agents Cytoskeletal Proteins DNA-Binding Proteins Intracellular Signaling Peptides and Proteins LIM Domain Proteins Neoplasms Vascular Diseases Animals Antineoplastic Agents Cytoskeletal Proteins Cytoskeletal Proteins DNA-Binding Proteins DNA-Binding Proteins Humans Intracellular Signaling Peptides and Proteins Intracellular Signaling Peptides and Proteins LIM Domain Proteins LIM Domain Proteins Mice Neoplasms

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