Peeling Skin Disorders: A Paradigm for Skin Desquamation

Has, Cristina

doi:10.1016/j.jid.2018.05.020

Cited by 23 publications

(23 citation statements)

References 11 publications

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“…Yet, if

is true then, in general, all absorbed dietary protein is only utilized for EE ; and thus, over time, total body protein persistently decreases because the EE -independent protein loss is not being compensated by dietary intake. EE -independent protein loss occurs in feces (e.g., excretion of mucin, an indigestible protein secreted by the intestinal mucosa [ 27 ]), in sweat (e.g., amino acids may be excreted during physical exertion [ 28 ]), in urine (e.g., urinary excretion of glycine in creatinine [ 29 ] and C-peptide [ 30 ], a 31 amino acid polypeptide generated from insulin secretion) and during renewal of skin, hair and nails (e.g., shedding of dead cells filled with keratin [ 31 , 32 , 33 ]). As a consequence, we run into a contradiction since body weight is simultaneously stable (true absorbed-oxidation identities imply mass balance) and decreasing (body protein is continuously diminishing).…”

Section: Methods and Resultsmentioning

confidence: 99%

Serious analytical inconsistencies challenge the validity of the energy balance theory

Arencibia-Albite¹

2020

Heliyon

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Energy metabolism theory affirms that body weight stability is achieved as over time the average energy intake equals the average energy expenditure, a state known as energy balance. Here it is demonstrated, however, that weight stability coexists with a persistent energy imbalance. Such unexpected result emerges as a consequence of the answers to three fundamental problems: 1. Is it possible to model body weight fluctuations without the energy balance theory? And if so, what are the benefits over the energy balance strategy? 2. During energy balance, how the oxidized macronutrient distribution that underlies the average energy expenditure is related to the macronutrient distribution of the average energy intake? 3. Is energy balance possible under a low-fat diet that simultaneously satisfies the following conditions? (a) The fat fraction of the absorbed energy intake is always less than the oxidized fat fraction of the energy expenditure. (b) The carbohydrate fraction of the absorbed energy intake is always greater or equal to the oxidized carbohydrate fraction of the energy expenditure. The first of these issues is addressed with the axiomatic method while the rest are managed through analythical arguments. On the whole, this analysis identifies inconsistencies in the principle of energy balance. The axiomatic approach results also in a simple mass balance model that fits experimental data and explains body composition alterations. This model gives rise to a convincing argument that appears to elucidate the advantage of low-carbohydrate diets over isocaloric low-fat diets. It is concluded, according to the aforementioned model, that weight fluctuations are ultimately dependent on the difference between daily food mass intake and daily mass loss (e.g., excretion of macronutrient oxidation products) and not on energy imbalance. In effect, it is shown that assuming otherwise may caused unintended weight gain.

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“…Yet, if

Section: Methods and Resultsmentioning

confidence: 99%

Serious analytical inconsistencies challenge the validity of the energy balance theory

Arencibia-Albite¹

2020

Heliyon

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“…Defects in corneodesmosome components themselves have been involved in corneodesmosome abnormality and lead to epidermal barrier impairment as follows: Abnormalities in genes encoding corneodesmosin can cause a generalized inflammatory type of peeling skin syndrome and those encoding desmoglein 1 can induce another generalized inflammatory type of peeling skin syndrome, SAM syndrome (severe skin dermatitis, multiple allergies, and metabolic wasting) [56,57].…”

Section: Desquamationmentioning

confidence: 99%

“…One of the well-known examples is the severe autosomal recessive form of ichthyosis, Netherton syndrome, caused by a defect in the serine-specific inhibitor Kazal type 5 (SPINK5) gene encoding LEKTI. Netherton syndrome has also been proposed as a generalized inflammatory type of peeling skin syndrome [56]. Lack of serine protease inhibition can increase activities of KLKs, thereby causing acceleration in the degradation of the corneodesmosome [57,58].…”

Section: Desquamationmentioning

confidence: 99%

Molecular Mechanism of Epidermal Barrier Dysfunction as Primary Abnormalities

Lee

2020

IJMS

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Epidermal barrier integrity could be influenced by various factors involved in epidermal cell differentiation and proliferation, cell-cell adhesion, and skin lipids. Dysfunction of this barrier can cause skin disorders, including eczema. Inversely, eczema can also damage the epidermal barrier. These interactions through vicious cycles make the mechanism complicated in connection with other mechanisms, particularly immunologic responses. In this article, the molecular mechanisms concerning epidermal barrier abnormalities are reviewed in terms of the following categories: epidermal calcium gradients, filaggrin, cornified envelopes, desquamation, and skin lipids. Mechanisms linked to ichthyoses, atopic dermatitis without exacerbation or lesion, and early time of experimental irritation were included. On the other hand, the mechanism associated with epidermal barrier abnormalities resulting from preceding skin disorders was excluded. The molecular mechanism involved in epidermal barrier dysfunction has been mostly episodic. Some mechanisms have been identified in cultured cells or animal models. Nonetheless, research into the relationship between the causative molecules has been gradually increasing. Further evidence-based systematic data of target molecules and their interactions would probably be helpful for a better understanding of the molecular mechanism underlying the dysfunction of the epidermal barrier.may not be the primary events in lesional skin. However, they can play a role in part as primary abnormalities because abnormalities in the epidermal barrier are already present in non-lesional skin of atopic dermatitis [1]. Epidermal trauma from tape stripping or irritant application also leads to initial disruption of the barrier, although the result at certain time points may be combined with compensatory reactions followed by trauma.Causative mechanisms involved in primary epidermal barrier dysfunction might be more valuable for the prevention of skin diseases induced by barrier abnormalities. However, the underlying mechanism has been discussed mainly in connection with immunologic responses, including cytokine production [1,9,10]. Accordingly, this review covers molecular mechanisms of epidermal barrier dysfunction as primary abnormalities by focusing on the causative factors of skin diseases (atopic dermatitis and ichthyoses) and experimental skin conditions (tape stripping and irritant application) associated with skin barrier abnormalities. Molecular Mechanisms Related to Epidermal Barrier DysfunctionFormation and maintenance of skin barrier integrity could be influenced by genetic and environmental factors involved in epidermal cell differentiation and proliferation, cell-cell adhesion, and skin lipids. Mechanisms related to epidermal barrier dysfunction at molecular levels have commonly illustrated filaggrin mutations [3,11]. Regarding the mechanism behind skin barrier integrity, the role of epidermal calcium gradients could be considered based on their influence on keratinocyte proliferation and dif...

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“…Despite differences in the susceptibility to infectious and inherited diseases of epithelial surfaces, such as staphylococcal scalded skin syndrome (Handler and Schwartz, 2014) and Netherthon syndrome (Proksch et al, 2008), external and internal integumentary epithelia share some aspects of gene expression. These aspects include induction of genes in the epidermal differentiation complex and genes encoding intercellular connections that point to common, yet so far incompletely characterized mechanisms of barrier function (Bragulla and Homberger, 2009;Has, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…Knockout studies of CDSN in mice showed a diminished integrity of corneodesmosomes leading to a detachment of the stratum corneum from the granular layers and lethal epidermal barrier defects in adult animals (Leclerc et al, 2009). In humans, loss-of-function mutations of CDSN result in severe skin barrier defects (Leclerc et al, 2009) and are causative for the peeling skin syndrome (Has, 2018).…”

Section: Introductionmentioning

confidence: 99%

The Differentiation-Associated Keratinocyte Protein Cornifelin Contributes to Cell-Cell Adhesion of Epidermal and Mucosal Keratinocytes

Wagner

Beer

Gschwandtner

et al. 2019

Journal of Investigative Dermatology

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Cornifelin (CNFN) has been identified as a protein component of epidermal corneocytes. Here, we investigated the tissue distribution of CNFN and potential consequences of CNFN deficiency on epithelial function in in vitro models of human skin and oral mucosa. Our detailed bioinformatics and immunostaining analysis revealed that CNFN is not only expressed in human epidermis but also in noncornifying oral mucosa. In normal epidermis, CNFN was confined to the upper granular layer and the stratum corneum. By contrast, in both partly cornifying and noncornifying oral mucosa, CNFN was expressed in a cell membraneeassociated pattern over several suprabasal layers. Small interfering RNAemediated knockdown of CNFN in epidermal keratinocytes (KCs) was associated with only subtle alterations of the overall epidermal architecture in skin models in vitro but led to altered morphology of corneodesmosomes, as detected by electron microscopy. Using dispase treatment followed by mechanical stress, epithelial sheets of CNFN-deficient epidermal KCs were easily disrupted, whereas their CNFN-competent counterparts remained intact. In contrast to the epidermal KCs, CNFN knockdown in oral KCs had a more severe effect and caused pronounced acantholysis in organotypic models of oral mucosa. Together, these findings indicate that CNFN is a structural component of the cell adhesion system of differentiated KCs in both epidermis and oral mucosa.

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Peeling Skin Disorders: A Paradigm for Skin Desquamation

Cited by 23 publications

References 11 publications

Serious analytical inconsistencies challenge the validity of the energy balance theory

Serious analytical inconsistencies challenge the validity of the energy balance theory

Molecular Mechanism of Epidermal Barrier Dysfunction as Primary Abnormalities

The Differentiation-Associated Keratinocyte Protein Cornifelin Contributes to Cell-Cell Adhesion of Epidermal and Mucosal Keratinocytes

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