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Review

CTIP2 and lipid metabolism: regulation in skin development and associated diseases

, &
Pages 1009-1017 | Received 06 Jul 2021, Accepted 02 Nov 2021, Published online: 17 Nov 2021
 

ABSTRACT

Introduction

COUP-TF INTERACTING PROTEIN 2 (CTIP2) is a crucial transcription factor exhibiting its control through coupled modulation of epigenetic modification and transcriptional regulation of key genes related to skin, immune, and nervous system development. Previous studies have validated the essential role of CTIP2 in skin development and maintenance, propagating its effects in epidermal permeability barrier (EPB) homeostasis, wound healing, inflammatory diseases, and epithelial cancers. Lipid metabolism dysregulation, on the other hand, has also established its independent emerging role over the years in normal skin development and various skin-associated ailments. This review focuses on the relatively unexplored connections between CTIP2-mediated control of lipid metabolism and alteration of EPB homeostasis, delayed wound healing, inflammatory diseases exacerbation, and cancer promotion and progression.

Areas covered

Here we have discussed the intricate interplay of various endogenous lipids and lipoproteins accompanying skin development and associated disease processes and the possible link to CTIP2-mediated regulation of lipid metabolism.

Expert opinion

Establishing the link between CTIP2 and lipid metabolism alterations in the context of skin morphogenesis and diverse types of skin diseases including cancer can help us identify novel targets for effective therapeutic intervention.

Article highlights

  • CTIP2 in skin morphogenesis, inflammatory skin diseases, cutaneous wound healing, and epithelial cancers.

  • CTIP2 as regulator of skin lipid metabolism to maintain EPB homeostasis.

  • Altered lipid metabolism dynamics in chronic inflammatory diseases.

  • Bioactive lipid mediators and lipoproteins as important regulators of cutaneous injury response pathway.

  • Lipids as central players in cancer biology.

Declaration of interest

A.K. Indra has received Industry support from Natural Product Inc and Natreon Inc. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was funded in part by a R15 grant (R15AR068584-01) to GI from National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and a R01 grant 5R01GM123081 (JX) from National Institute of General Medical Sciences at National Institutes of Health (NIH), USA.

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