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Skin Structure & Function

Updated: Sep 14, 2023

It shouldn’t be a surprise that the first thing we recognize when we look at someone is their skin. Even though we might reckon noticing the eyes or a friendly smile first, our brain has already developed a rudimentary assessment and assumption of that individual’s racial group, health status or hygiene. The Skin, however, hasn’t been given much of an organ spotlight as say the Brain, despite being the body’s largest. We will quickly realize in this first Skin Science Blog that this organ is more than skin deep, more than what meets the eye. Beyond the mere Physical Barrier skin provides, as it demarcates internal from external, skin boasts a plethora of functional properties necessary for our survival. These range from Immune defence, Heat Regulation, Moisture Retention, Sensation Detection, to Vitamin D Synthesis. The complement of Skin Function (i.e., Skin Anatomy), encompasses structures such as hair, nails, sweat (sudoriferous) glands and oil (sebaceous) glands all having their unique duties.

Figure 1. Basic Skin Structure. Image by pikisuperstar on Freepik

This collective of functional subsystems and auxiliary structures is referred to by skin science professionals as the Integumentary System. We will keep things simple in this blog and work with ‘Skin’ for now.

The Skin Layers

Skin has two (2) layers, an outer layer called Epidermis and a layer beneath termed Dermis. There is an interesting region underneath the dermis that skin anatomists don’t consider being ‘skin-like’ or cutaneous in nature, and have settled on referring to this region as Subcutaneous tissue or Hypodermis.


This is the layer that is visible and which we apply skin care products on. Commonly, this outer layer is referred to as Skin, but in fact, we’ve only scratched the surface. In the meantime, let us explore the epidermis and its 4-5 sandwich-like sublayers, with each layered region satisfying specific duties or functions of: i. barrier defence; ii. water retention; iii. pigmentation (skin colour); and iv. sensation detection (fine touch, pressure, vibration). Anatomists have given two-part Latin names (Nomenclature) to these 4-5 layers (strata), with each name beginning with “Stratum”. From outer to inner, these are known as: 1. Stratum Corneum, 2. Stratum Lucidum (only present in palms of hands and soles of feet [plantopalmar skin]), 3. Stratum Granulosum, 4. Stratum Spinosum and 5. Stratum Basale. Advancements in Dermatology called for the need to further ascertain region-specific structures, functions and biochemical processes. Because of this, layers like Stratum Corneum are subdivided into Stratum Compactum and Stratum Disjunctum. More commonly, however, the terms upper and lower are used in place of the Latin names for some of the other strata which we will soon discuss in depth.

Figure 2. Sublayers of the Epidermis. Skin Tissue Engineering. Wong DJ, Chang HY. (2019)


The dermis seats just beneath and is stitched to the overlying epidermis by protein rivets called Hemidesmosomes, without which the epidermis would completely slough off after a routine shower. The interface of dermis and epidermis is referred to as the Dermal-Epidermal Junction and can be seen under light microscopy as an undulating interdigitation of dermis and epidermis (Dermal Papillae & Rete Ridges), necessary to withstand shear forces. Dermis is further divided into two layers: 1. a highly vascularized, thin connective tissue meshwork of loosely packed Type I and Type III collagen called the Papillary Layer; and a contrasting 2. thick connective tissue layer of densely packed collagen known as the Reticular Layer. Notable structures found in the dermis include blood vessels (which are absent in the epidermis); varying types of Sensory Receptors (pacinian corpuscles, ruffini’s corpuscles, meisnner’s corpuscles, thermoreceptors, norciceptors); Sweat Glands (apocrine, eccrine); Pilosebaceous Units (hair follicle and sebaceous gland); and Lympathics. Also resident in this layer are special structures called Dermal Fibroblasts, which are tiny cell factories that manufacture fibrous scaffolding (Collagen and Elastin), offering support, strength, and flexibility to the overlying epidermis. Fibroblasts are essential for skin's plumpness. As we age skin becomes less supple, wrinkled, and prone to everyday insults. This is due to the progressive decrease in activity of these Dermal Fibroblasts as well as reduced production of youthful compounds such as elastin, collagen, hyaluronic acid and chondroitin. [1] In future posts we will address aging in more depth (Chronological vs. Biological Aging; Photoaging; Anti-aging Skin Care Technology etc.).

Hypodermis/Subcutaneous Tissue

While not considered cutaneous or skin-like, this region underneath Skin Proper (Epidermis and Dermis) have some note worthy roles to play. Hypodermis is made up mostly of fatty tissue and blood vessels that ensure thermal insulation and temperature regulation. It also serves as a shock absorbing cushion, protecting deeper (visceral) organs against blunt trauma. Skin contouring and appearance are partially attributed to this layer’s body fat stores. Excess stored fat can cause skin to appear lumpy or dimpled, as sometimes seen on the back of thighs for example; while very low body fat percentages can cause skin to appear less plump, flat and dry.


Skin has a surface area of about 20sq.ft, roughly the size of a picnic blanket.


Epidermis in Focus

Keratinocyte Life Cycle

We will begin discussing in depth the Epidermal sublayers and their functions in the context of a Keratinoctye’s (skin cell) journey up through the sublayers— from bottom (Stratum Basale) to top (Stratum Corneum). As a guiding concept, a Keratinocyte’s fate is to relinquish its vital force (Programmed Cell Death) to become a flattened, deactivated skin cell called a Corneocyte. The mini saga of a Keratinocyte’s Life Cycle begins with: 1. (Proliferation) an expansion in cell number as keratinocyte-stem cells mitotically clone themselves; 2. (Terminal Differentiation) structural and physiological modifications to the Keratinocyte necessary for transformation into a Corneocyte; and 3. (Desquamation) sloughing away or shedding of Corneocytes into the environment.

This entire sequence of events referred to as Epidermal Turnover which takes on average 28 days or about 4 weeks. [2]


When testing out skin care products, this important fact should be considered in order to make sound judgement on Performance Efficacy.


Along this rather complex and dynamic journey, we will stumble upon instances where physiological processes could become disordered or dysregulated (Pathophysiology) due to external factors (e.g., UV Damage) or internal ones (e.g., Genetic Mutation)— phenotypically presenting as common Skin Disease States or Dermatoses like Atopic Dermatitis (Eczema).


Figure 3. Layers of the Epidermis. Art Illustration by Elizabeth Lander,

Stratum Basale

S. Basale is the lowest and thinnest of the epidermal layers comprising of a single row of packed cuboidal to low columnar cells fastened to each other by protein buttons called Desmosomes. Desmosomes confer horizontal strength and rigidity to the layer, while Hemidesmosomes resist shear forces by anchoring these cells to an underlying basement of specialized extracellular matrix called the Basement Membrane. This structure serves as a sturdy platform on which overlying epidermal layers can be sequentially stacked on top of, as well as compartmentalizing Dermis from Epidermis. S. Basale, compared to the other epidermal layers has high cellular activity when observed microscopically. Keratinocytes of this first region continuously clone themselves by Mitosis, pushing up and away older cells and making space for the new (Cellular Proliferation). For this reason, S. Basale is also known as Stratum Germinativum, to reflect the germinative quality of keratinocytes in this layer.

Stratum Basale is comprised of three (3) types of cells: Melanocytes, Keratinocytes and Merkel Cells. Melanocytes, which account for 5% of all epidermal cells, are responsible for a pigment you might have heard of called Melanin. This pigment gets synthesized inside a specialized cell compartment known as the Melanosome. Melanocytes send out tentacle-like projections between overlying keratinocytes (at the interstices) that contain the pigment— keratinocytes take up this pigment. Melanin is to our skin as Chlorophyll is to leaves and allows for the many wonderful hues of skin colour we see around the globe as well as offering the boon of moderate UV Ray (UVR) protection by forming a dome-shaped pigmented covering over the nuclei of keratinocytes (Melanin Barrier/Photoprotection Barrier). [2,3] The hues of skin colour depends on how much melanin pigment is produced (cellular activity) rather than melanocyte quantity. Keratinocytes, as we will soon realize are the default residents of the skin constituting up to 85% of total epidermal cell count and are stars of the show (Keratinocyte Life Cycle). [3] Skin’s Permeability Barrier (physical barrier, waterproofing) is also attributed to keratinocytes among other structural players. Merkel Cells, after German Anatomist Friedrich Merkel, are mechanoreceptors that detect touch sensations which allow us to be aware of what comes in contact with our skin and account for 6-10% of epidermal cell abundance. [3]


The Fitzpatrick Scale of Skin Phototypes was stipulated by dermatologist Thomas B. Fitzpatrick in 1975 as a model to determine sun sensitivity (tanning tendency) in relation to skin colour.


Stratum Spinosum

Stratum Spinosum, also known as the Prickle-Cell Layer, is the second layer up from S. Basale and is the thickest of the epidermal layers (8-10 cell layers). Skin scientists have divided this layer into an upper and lower region based on special physiological and biochemical processes specific to these regions. Overall, the role of S. Spinosum is to set stage for the grand events of Terminal Differentiation (Cornification/Keratinization). A major preparatory step is the retention of adequate skin moisture levels that facilitate complex physiological mechanisms of terminal differentiation. A fishnet-like mesh made of the structural protein called Keratin, ensures adequate moisture trapping that manifests as supple skin with good elasticity. Keratin Intermediate Filaments are the skeletal frame of the cell (cytoskeleton), offering a keratinocyte internal strength and rigidity much like the body’s Skeletal System proper. Later on, when we discuss Stratum Granulosum, we will notice that as the keratinocyte terminally differentiates, these intermediate filaments hardened and bundle together to aid skin’s Permeability Barrier (e.g., waterproofing).

The body’s first line of Immune Defence takes up post on this stratum as sentinel Langerhans cells (5% of cells in the epidermis). [3] These skin specific, tissue-resident macrophages continually sample foreign particulates like microbes and allergens, digest them by receptor-mediated endocytosis or present them to other immune players to initiate coordinated responses. (In some, this immunological response is or can become dysregulated or uncoordinated resulting in a cascade of inflammatory issues, as seen in Eczema or Rosacea. [2,7,8]

Let us now take a look at the biochemical processes of this layer, particularly in the Upper Stratum Spinosum, keeping in mind that these processes are preparatory events of Terminal Differentiation, (i.e., the conversion of Keratinocyte into Corneocyte, Cornification/Keratinization).[2] As a conceptual overview, Cornification results in two (2) major structural modifications of the keratinocyte’s plasma membrane: 1. (Protein Modification) development of a Cornified Cell Envelope; and 2 (Lipid Modification) development of Multilamellar Lipid Structure. These modifications will be addressed in more detail soon. At the Upper Spinosum, cellular machinery such as Free Ribosomes and packaging houses like the Golgi Apparatus, manufacture subcellular structures that 'sound off' the cornification process, these structures are Keratohyalin Granules and Odland Bodies, respectively. Keratohyalin Granules (which have their final resting place at Stratum Granulosum) are cytosol-based, insoluble protein granules that harbour smaller precursor proteins such as: profilaggrin, tricohyalin, loricin and keratin. These precursor players confer protein modifications to the keratinocyte membrane.

Odland Bodies are pouch-like repositories which also have their resting place at S. Granulosum (where they are referred to as Lamellar Bodies); and contain Precursor Lipids (cholesterol sulfate, glucosyl ceramides, sphingolipids and phospholipids) as well as Lipid-Assembly Enzymes (acidic sphingomyelinase, secretory phospholipase A2) that confer lipid modifications to the keratinocyte membrane. Odland/Lamellar Bodies may also contain other biochemical and immunological players, namely: kallikrein, cathepsin, corneodesmosin, proteases and beta 2 defensins). [2,3]

Skin scientists have discovered a gradient of intracellular calcium (Ca2+) at the Spinosum layer, with Upper S. Spinosum having elevated Ca2+ levels compared to Lower S. Spinosum. This inherent difference in concentration is what initiates early enzymatic mechanisms of Cornified Cell Envelope development— (by activating Transglutaminase 1 [TGase 1] and crosslinking major structural proteins. Developmental activity reaches its peak at S. Granulosum).

Stratum Granulosum

Being the next layer up from S. Spinosum and the thinnest (3-5 cell layers), Stratum Granulosum demarcates moisture rich bottom layers—S. Basale; S. Spinosum—from moisture-poor upper layers—S. Lucidum (plantopalmar skin); S. Corneum. Histologically, this layer appears granular due to the abundance of aggregated keratohyalin granules present in the cytosol of keratinocytes. The big picture here at this stratum is elevated keratinocyte modification activity (Cornification process), not only to the plasma membrane but to the rest of the skin cell as well. These global cellular changes are mainly made possible by Keratin Filaments. Keratin filamentous proteins start becoming hardened, flattened, and bundled together— a process that reaches its peak at Upper S. Granulosum. Intermediate-associated proteins like tricohyalin and filaggrin become activated, allowing for water repellence and reduced Trans Epidermal Water Loss (TEWL). This phenomenon, TEWL, can be described as the passive evaporation of moisture from skin due to differences in water vapour pressures between our body and the atmosphere.[2] In general, our body water would much rather seep out into the environment than stay in, but if allowed to do so can cause us to literally shrivel up and die. Skin has the important task of ensuring such a disaster does not happen. In some instances, above-threshold water loss does occur resulting in a host of dry skin conditions collectively referred to as Xerosis.

The Cornification process continues, as the keratinocyte sequentially forms its most important structure called the Cornified Cell Envelope. This envelope is a result of both Protein and Lipid Modifications. The protein modification leg begins with the linking of several proteins to build a scaffold-like supportive structure for lamellar lipids in addition to serving as a protective physical barrier against injury. Recall from the previous stratum how Ca2+ gradients activated Transglutaminase 1 (TGase 1), well, this process continues here at S. Granulosum as TGase 1 enzyme crosslinks a series of proteins—(loricrin, cystatin, small proline-rich proteins [SPRs] desmoplakin, involucin, elafin, filaggrin, envoplakin, cornifin, type 2 keratins, and desmoglein)— to form of a monomolecular layer of acylglucosylceramides beneath the plasma membrane. Acylglucosylceramide (an omego-hydroxyceramide derivative) forms a sturdy support for the future deposition of multilamellar lipids on the keratinocyte cell surface (Lipid Modification). [2,3]

Lipid Modification is underway once the lipid triad (Ceramides, Cholesterol & Free Fatty Acids) of Odland bodies have sufficiently matured (enzymatically processed). Only then can these lipids be extruded by exocytosis from their pouches and deposited on top of the plasma membrane. Multilamellar lipids are made up of about 40%-50% Ceramides, 25% Cholesterol, 10-15% Free Fatty Acids, with the remainder being simple lipids (neutral or true lipids). [2]


The quantity as well as quality of Ceramides, which are the most abundant of the lipid triad, is essential to the health of the Multilamellar Lipid Structure, especially since Ceramides can only be obtained nutritionally.


Interestingly, extracellular pH steadily starts dropping from a neutral pH of 7, gradually getting more acidic up through S. Corneum, eventually setting up a skin surface pH of 4.5 (Skin Acid Mantle) that renders the surface inhabitable for most harmful pathogens. There is increased activity at Upper Stratum Granulosum as several events happen concomitantly that ultimately complete the Cornification/Keratinization Process. This region, straddled between Lower S. Granulosum and Stratum Corneum (S. Disjunctum), is referred to as the Transitional Zone and marks the transition of a Keratinocyte becoming a Corneocyte. A major occurrence at this zone is the formation of Natural Moisturizing Factors (NMFs), which are high molecular weight hydrophilic compounds which have strong binding affinity to water— (they can hold on to moisture in the skin or even trap moisture from the atmosphere). These compounds are crucial to skin’s natural hydration, by reducing Trans Epidermal Water Loss, and facilitating Keratinization/Cornification.[2]

Exactly how these water binding compounds are made begins with a convergence of factors. The enzyme Caspase 14 in the presence of elevated Ca2+ levels and a low pH (acidic environ) cause the degranulation of keratohyalin granules and release of dormant profilaggrin into the keratinocyte cytoplasm. Profilaggrin is freely activated (uninhibited) spontaneously converting to Filaggrin. A fraction of filaggrin protein dissociate to form amino acid derivatives— Natural Moisturizing Factors— such as amino acids, pyrrolidone carboxylic acid (PCA), lactate and uronic acid. [2,3]

With the availability of filaggrin, as well as other intermediate filament-associated proteins like trichohyalin, keratinization is made possible. Filament-associated proteins induce the aggregation of keratin filaments (Tonofilaments) into keratin bundles (Tonofibrils).[3] Tonofibrils further harden the cell providing rigidity and reinforcement to the water barrier. (The water barrier is partly mounted by the deposition of multilamellar lipids by Lamellar Bodies on the plasma membrane and between cells). Keratinocytes lose their nucleus and most of their cellular machinery (organelles) that sustain vital processes, becoming deactivated, but not entirely lifeless— as was the popular belief among skin scientists of old. Cornification is now complete thanks to the formation of the Cornified Cell Envelope and Cellular Deactivation. The keratinocyte undergoes a name change to Corneocyte, at which point the region containing these specialized cells also undergoes a name change, Stratum Corneum.

Stratum Lucidum

Stratum Lucidum only makes an appearance in palmoplantar skin (i.e., skin of the palms of hands and soles of feet), where robustness is needed. Anatomists use the term ‘thick skin’ to refer to palmoplantar skin and ‘thin skin’ for the rest of the body skin regions. This layer is just about the same in thickness as S. Granulosum (~3-5 cell layers). It is believed by some skin scientists that Stratum Lucidum can make an appearance in ‘thin skin’ in cases of Pruritic (itchy) Eczema— an eczematous variant with a strong urge to scratch. In this form of eczema, it is stipulated that ‘thin skin’ tries to protect itself from high-shear scratching by forming an extra leathery layer that is Stratum Lucidum-like. This explains why the skin of those affected with Atopic Dermatitis struggle with skin roughness, constantly seeking hypoallergenic moisturizers and body lotions with good emollience which can soften, smooth and sooth their skin. We will dive deep into Eczema as a skin malady in a future post on Common Skin Pathologies. At this layer also, keratinocytes are virtually devoid of life and start densely packing together, working along with Stratum Granulosum to enhance the waterproofing effect.

Stratum Corneum

We have finally reached the last and outermost of the epidermal layers, Stratum Corneum. Like some of the other epidermal layers, this stratum is divided into a Lower and Upper region, called Stratum Compactum and Stratum Disjunctum respectively. Stratum Compactum captures the final events of Cornification within the Transitional Zone as well as the other events of Compaction. Compaction involves the stitching together of these specialized corneocytes (also known as Squames). To do so, tonofibrils— formed as a result of the cornification/keratinzation process— take on the role as specialized protein rivets called Corneodesmosomes that stitch adjacent corneocytes together in a serrated fashion (Corneocyte Compaction).[3] This process is essential to the integrity of skin’s barrier defence fronts, particularly its Permeability Barrier, by preventing the free passage of pathogens, allergens and other invaders, in addition to preventing TEWL. Incomplete Corneocyte Compaction can result from a faulty Cornification Process (i.e., poor Cornified Cell Envelope formation) usually due to filaggrin protein deficiency (Filaggrin Mutagenesis).[2] We will dive deeper into the pathophysiology of incomplete cornification in a future post.

At Stratum Disjunctum (Upper S. Corneum), skin cells meet their fate after dutifully serving their purpose of Barrier Defence and must now be shed from the body to allow for new replacements. This replacement of old with new happens by an intricately complex process of enzymatic dissolution at the level of the corneodesmosomes. Desquamation is the term used to describe this event, as squames (corneocytes) slough off into the environment— a process initiated by an acidic pH environment and proteolytic enzymes like Cathepsin and Kallikrein Serine Proteases (KLK5, KLK7, KLK14). This complex process of shedding must be carefully regulated to prevent excess, partial or even under shedding. This is accomplished by regulating the proteolytic enzymes of desquamation (cathepsin, kallikrein serine proteases) using pH dependent protease inhibitors such as Lymphoepithelial Kazal-Type Inhibitor (LEKTI) and Cholesterol Sulfate.[2,3,6]

Homeostatic balance of desquamation ensures proper Stratum Corneum thickness and a viable Physical Barrier Defence. The rate of corneocyte shedding increases moving up from lower to upper S. Corneum regions. The visible evidence of orderly desquamation appears under light microscopy as a ‘honeycomb’, which is actually the patterned structural remains of cornification. Adequate hydration throughout S. Corneum facilitates this intricate process. Disorderly or incomplete desquamation, sometimes seen in extremely dry, xerotic skin can result in the clumping or build-up of unseparated squames appearing ‘scaly’ in nature, thereby compromising barrier integrity and increasing penetration susceptibility of exogenous factors. The fine balance of desquamation (between pro and inhibitory enzymes) is a marvel of Stratum Corneum.

In closing, it has been the pursuant scientific work of Corneobiologists, Dermatologists and other Skin Scientists alike that have shed light on the wonders of this epidermal layer, and the Integumentary System at large, thereby paving the way for advancements in modern Skin Care Formulations.

Pick up on the Skin Science Saga with our next blog, Skin Barrier Defence.

-Samuel Jones

Bsc. Biological Sciences (Hons.)

PG. Dip. Organic Personal Care/Cosmetic Science

PG. Cert. Barrier Disordered Skin

PG. Cert. Beekeeping




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