Abstract
Hereditary blistering skin diseases were described more than hundred years ago, but only the rapid scientific developments in molecular genetics in the last years have revealed the full spectrum of these diseases, delineated disease mechanisms and pointed to novel therapeutic strategies. Not only the classic forms of epidermolysis bullosa, but also new syndromic forms with multiorgan involvement, or skin fragility disorders that manifest with erosive, crusty lesions and pigment anomalies, instead of marked skin blistering belong to the group of hereditary blistering diseases. Understanding the biological functions of skin structures that provide intraepidermal and dermo-epidermal adhesion has furthered development of novel cell- and molecule-based therapies that are currently being tested in preclinical and clinical pilot trial settings.
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