Role of mTOR Signaling Cascade in Epidermal Morphogenesis and Skin Barrier Formation

The skin epidermis, with its capacity for lifelong self-renewal and rapid repairing response upon injury, must maintain an active status in metabolism. Mechanistic target of rapamycin (mTOR) signaling is a central controller of cellular growth and metabolism that coordinates diverse physiological an...

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Published inBiology (Basel, Switzerland) Vol. 11; no. 6; p. 931
Main Authors Wang, Juan, Eming, Sabine A., Ding, Xiaolei
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 19.06.2022
MDPI
Subjects
Animal models
Autophagy
Biosynthesis
Cell differentiation
Cell growth
Cell proliferation
Cell self-renewal
epidermal morphogenesis
Epidermis
Epithelium
Growth factors
Insulin
Keratinocytes
Kinases
Metabolism
Morphogenesis
mouse models
mTOR
Mutation
Physiology
Protein kinase
Proteins
Rapamycin
Regulation
Review
Reviews
skin barrier
Skin diseases
TOR protein
Transgenic mice
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Abstract The skin epidermis, with its capacity for lifelong self-renewal and rapid repairing response upon injury, must maintain an active status in metabolism. Mechanistic target of rapamycin (mTOR) signaling is a central controller of cellular growth and metabolism that coordinates diverse physiological and pathological processes in a variety of tissues and organs. Recent evidence with genetic mouse models highlights an essential role of the mTOR signaling network in epidermal morphogenesis and barrier formation. In this review, we focus on the recent advances in understanding how mTOR signaling networks, including upstream inputs, kinases and downstream effectors, regulate epidermal morphogenesis and skin barrier formation. Understanding the details of the metabolic signaling will be critical for the development of novel pharmacological approaches to promote skin barrier regeneration and to treat epidermal barrier defect-associated diseases.
AbstractList The skin epidermis, with its capacity for lifelong self-renewal and rapid repairing response upon injury, must maintain an active status in metabolism. Mechanistic target of rapamycin (mTOR) signaling is a central controller of cellular growth and metabolism that coordinates diverse physiological and pathological processes in a variety of tissues and organs. Recent evidence with genetic mouse models highlights an essential role of the mTOR signaling network in epidermal morphogenesis and barrier formation. In this review, we focus on the recent advances in understanding how mTOR signaling networks, including upstream inputs, kinases and downstream effectors, regulate epidermal morphogenesis and skin barrier formation. Understanding the details of the metabolic signaling will be critical for the development of novel pharmacological approaches to promote skin barrier regeneration and to treat epidermal barrier defect-associated diseases.
Simple SummaryThe skin epidermis is a stratified multilayered epithelium that provides a life-sustaining protective and defensive barrier for our body. The barrier machinery is established and maintained through a tightly regulated keratinocyte differentiation program. Under normal conditions, the basal layer keratinocytes undergo active proliferation and migration upward, differentiating into the suprabasal layer cells. Perturbation of the epidermal differentiation program often results in skin barrier defects and inflammatory skin disorders. The protein kinase mechanistic target of rapamycin (mTOR) is the central hub of cell growth, metabolism and nutrient signaling. Over the past several years, we and others using transgenic mouse models have unraveled that mTOR signaling is critical for epidermal differentiation and barrier formation. On the other hand, there is increasing evidence that disturbed activation of mTOR signaling is significantly implicated in the development of various skin diseases. In this review, we focus on the formation of skin barrier and discuss the current understanding on how mTOR signaling networks, including upstream inputs, kinases and downstream effectors, regulate epidermal differentiation and skin barrier formation. We hope this review will help us better understand the metabolic signaling in the epidermis, which may open new vistas for epidermal barrier defect-associated disease therapy.AbstractThe skin epidermis, with its capacity for lifelong self-renewal and rapid repairing response upon injury, must maintain an active status in metabolism. Mechanistic target of rapamycin (mTOR) signaling is a central controller of cellular growth and metabolism that coordinates diverse physiological and pathological processes in a variety of tissues and organs. Recent evidence with genetic mouse models highlights an essential role of the mTOR signaling network in epidermal morphogenesis and barrier formation. In this review, we focus on the recent advances in understanding how mTOR signaling networks, including upstream inputs, kinases and downstream effectors, regulate epidermal morphogenesis and skin barrier formation. Understanding the details of the metabolic signaling will be critical for the development of novel pharmacological approaches to promote skin barrier regeneration and to treat epidermal barrier defect-associated diseases.
Author Eming, Sabine A
Wang, Juan
Ding, Xiaolei
AuthorAffiliation 6 Institute of Zoology, Developmental Biology Unit, University of Cologne, 50674 Cologne, Germany
1 Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People’s Hospital of Nantong), School of Medicine, Shanghai University, Nantong 226011, China; juanw@shu.edu.cn
2 Shanghai Engineering Research Center of Organ Repair, School of Medicine, Shanghai University, Shanghai 200444, China
5 Center for Molecular Medicine Cologne (CMMC), University of Cologne, 50931 Cologne, Germany
4 Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50674 Cologne, Germany
3 Department of Dermatology, University of Cologne, 50937 Cologne, Germany
AuthorAffiliation_xml – name: 4 Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, 50674 Cologne, Germany
– name: 3 Department of Dermatology, University of Cologne, 50937 Cologne, Germany
– name: 5 Center for Molecular Medicine Cologne (CMMC), University of Cologne, 50931 Cologne, Germany
– name: 2 Shanghai Engineering Research Center of Organ Repair, School of Medicine, Shanghai University, Shanghai 200444, China
– name: 1 Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People’s Hospital of Nantong), School of Medicine, Shanghai University, Nantong 226011, China; juanw@shu.edu.cn
– name: 6 Institute of Zoology, Developmental Biology Unit, University of Cologne, 50674 Cologne, Germany
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Snippet The skin epidermis, with its capacity for lifelong self-renewal and rapid repairing response upon injury, must maintain an active status in metabolism....
Simple SummaryThe skin epidermis is a stratified multilayered epithelium that provides a life-sustaining protective and defensive barrier for our body. The...
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SubjectTerms Animal models
Autophagy
Biosynthesis
Cell differentiation
Cell growth
Cell proliferation
Cell self-renewal
epidermal morphogenesis
Epidermis
Epithelium
Growth factors
Insulin
Keratinocytes
Kinases
Metabolism
Morphogenesis
mouse models
mTOR
Mutation
Physiology
Protein kinase
Proteins
Rapamycin
Regulation
Review
Reviews
skin barrier
Skin diseases
TOR protein
Transgenic mice
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Title Role of mTOR Signaling Cascade in Epidermal Morphogenesis and Skin Barrier Formation
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