My primary research activities involve the area of extracellular matrix. In particular, my studies focus on (i) identifying pathomechanisms of heritable diseases of connective tissues caused by mutations in collagen genes, (ii) technologies to produce novel collagen-like proteins for biomedical applications, and (iii) developing novel approaches to limit excessive fibrosis.

In the studies on the molecular basis of the heritable diseases caused by mutations in collagenous proteins, my studies place a main emphasis on (i) osteogenesis imperfecta caused by mutations in collagen I, (ii) spondyloepiphyseal displasias caused by mutations in collagen II, and (iii) on epidermolysis bullosa caused by mutations in collagen VII.

In addition to the studies on pathomechanisms of heritable diseases of connective tissues, my work contributed significantly to developing novel technologies for the production of human recombinant collagens for a number of biomedical applications. As animal-derived collagens and gelatin, at present widely used in biomedical and pharmaceutical fields, have the potential to transmit animal-derived diseases, the ability to produce recombinant human collagens and gelatin is very attractive. The high value and the potential applicability of recombinant human collagens are reflected by an approved patent and its licensing by Thomas Jefferson University to a commercial company. In addition to already established technologies, I continue developing new approaches to the rational engineering of collagenous proteins for biomedical applications. In response to the need for novel therapies for fibrotic diseases, my laboratory has recently initiated studies on novel approaches to limit excessive fibrosis. These new approaches are built on my discoveries of processes that govern the formation of collagen fibrils. As this process is fundamental for the formation of fibrotic deposits, my concept is that, by inhibiting the formation of collagen fibrils, it will be possible to limit fibrosis. If experimentally confirmed, this novel concept may lead to developing novel inhibitors of fibrotic processes occurring in keloids, hypertrophic scarring, and others.