Thesis supervisor: Péter Hamar
Location of studies (in Hungarian): PTE ÁOK Pécs, Szigeti u. 12. Abbreviation of location of studies: ÁOK
Description of the research topic:
Renal transplantation offers the best quality of life in renal failure patients. The development of surgical techniques, modern immunosuppression and supportive therapies improved prognosis significantly in the past decades. Thus, presently the leading cause of graft loss is a process previously called chronic rejection but recently described as interstitial fibrosis and tubular atrophy (IFTA). Several factors are involved in the development of IFTA such as early damage of the graft due to ischemia-reperfusion injury, increased work-load on the sole kidney and alloantigen dependent, subclinical rejection episodes. Furthermore, chronic processes such as chronic inflammation culminating in fibrotic, scaring tissue-remodelling and graft failure.
We utilize rodent (rat, mouse) models (orthotopic kidney transplantation, ischemia-reperfusion injury, fibrosis) and human material (registry data, biobank-samples) to investigate the driving processes of renal fibrosis, focusing on small-, protein-non-coding RNAs. Exogenous short interfering RNAs (siRNA) are capable of inhibiting the synthesis of specific proteins, whereas influencing the synthesis of endogenous micro RNAs (miRNA) the role of whole signaling cascades can be investigated.
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