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Agic, Mediha Becriovic
Alternative names
Publications (3 of 3) Show all publications
Hultström, M., Becriovic-Agic, M. & Jönsson, S. (2018). Comparison of acute kidney injury of different aetiology reveals in-common mechanisms of tissue damage. Physiological Genomics, 50(3), 127-141
Open this publication in new window or tab >>Comparison of acute kidney injury of different aetiology reveals in-common mechanisms of tissue damage
2018 (English)In: Physiological Genomics, ISSN 1094-8341, E-ISSN 1531-2267, Vol. 50, no 3, p. 127-141Article, review/survey (Refereed) Published
Abstract [en]

Acute kidney injury (AKI) is a syndrome of reduced glomerular filtration rate (GFR) and urine production caused by a number of different diseases. It is associated with renal tissue damage. This tissue damage can cause tubular atrophy and interstitial fibrosis that leads to nephron loss and progression of chronic kidney disease (CKD). This review describes the in-common mechanisms behind tissue damage in AKI caused by different underlying diseases. Comparing six high-quality microarray studies of renal gene expression after AKI in disease models (gram-negative sepsis, gram-positive sepsis, ischemia-reperfusion, malignant hypertension, rhabdomyolysis and cisplatin toxicity) identified 5254 differentially expressed genes in at least one of the AKI models. 66% of genes were only found in one model showing that there are unique features to AKI depending on the underlying disease. There were in-common features in the form of four genes that were differentially expressed in all six models, 49 in at least five, and 215 were in-common between at least four models. Gene ontology enrichment analysis could be broadly categorized into the injurious processes hypoxia, oxidative stress, and inflammation, as well as the cellular outcomes of cell death and tissue remodeling in the form of epithelial to mesenchymal transition (EMT). Pathway analysis showed that MYC is a central connection in the network of activated genes in-common to AKI, which suggests that it may be a central regulator of renal gene expression in tissue injury during AKI. The outlining of this molecular network may be useful for understanding progression from AKI to CKD.

Keywords
acute kidney injury, biomarker, gene expression, molecular, tissue injury
National Category
Physiology
Research subject
Physiology
Identifiers
urn:nbn:se:uu:diva-340389 (URN)10.1152/physiolgenomics.00037.2017 (DOI)000428814500001 ()29341864 (PubMedID)
Funder
Swedish Society for Medical Research (SSMF)
Available from: 2018-01-29 Created: 2018-01-29 Last updated: 2018-08-14Bibliographically approved
Becriovic Agic, M., Jönsson, S. & Hultström, M. (2017). Genetic association of oxidative stress and fluid accumulation makes Balb/CJ mice more sensitive to decompensated heart failure. Acta Anaesthesiologica Scandinavica, 61(8), 963-964
Open this publication in new window or tab >>Genetic association of oxidative stress and fluid accumulation makes Balb/CJ mice more sensitive to decompensated heart failure
2017 (English)In: Acta Anaesthesiologica Scandinavica, ISSN 0001-5172, E-ISSN 1399-6576, Vol. 61, no 8, p. 963-964Article in journal, Meeting abstract (Other academic) Published
Place, publisher, year, edition, pages
WILEY, 2017
National Category
Anesthesiology and Intensive Care
Identifiers
urn:nbn:se:uu:diva-342121 (URN)000407231100016 ()
Available from: 2018-02-22 Created: 2018-02-22 Last updated: 2018-02-22Bibliographically approved
Jönsson, S., Agic, M. B., Tveitaras, M., Skogstrand, T., Karlsen, T. V., Lidén, Å., . . . Hultström, M. (2015). C57BL/6J mice are resistant to cardiorenal syndrome during high-salt and Angiotensin II treatment compared to Balb/c because of higher oxidative stress. Acta Physiologica, 215, 85-85
Open this publication in new window or tab >>C57BL/6J mice are resistant to cardiorenal syndrome during high-salt and Angiotensin II treatment compared to Balb/c because of higher oxidative stress
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2015 (English)In: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 215, p. 85-85Article in journal, Meeting abstract (Other academic) Published
National Category
Physiology
Identifiers
urn:nbn:se:uu:diva-284883 (URN)000370526500115 ()
Available from: 2016-04-19 Created: 2016-04-19 Last updated: 2018-01-10Bibliographically approved
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