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Role of hypoxia‐inducible factor 1α as a potential biomarker for renal diseases—A systematic review
Author(s) -
Encinas Jéssica Freitas Araújo,
Foncesca Carlos Henrique,
Perez Matheus Moreira,
Simões Diogo Pimenta,
Costa Aguiar Alves Beatriz,
Bacci Marcelo Rodrigues,
Maifrino Laura Beatriz Mesiano,
Fonseca Fernando Luiz Affonso,
Veiga Glaucia Luciano
Publication year - 2019
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3425
Subject(s) - hypoxia inducible factors , hypoxia (environmental) , disease , kidney , biomarker , homeostasis , kidney disease , medicine , biology , bioinformatics , pathology , chemistry , biochemistry , gene , oxygen , organic chemistry
Renal cells need oxygen for homeostasis; it is known for adjusting cellular functioning and the energy obtainment have a broad relationship with cellular respiration, through the O 2 bioavailability. O 2 homeostasis regulation in the kidney is mediated by hypoxia‐inducible factors (HIFs). HIF is divided into three α isoforms, represented by HIF‐1α, HIF‐2α, and HIF‐3α in addition to three paralogs of HIF‐1β; these are involved in some metabolic processes, as well as in the pathogenesis of several diseases. Renal biopsy analyses of patients and experimental animal models aim to understand the relationship between HIF and protection against developing renal diseases or the induction of their onset, being thus this molecule can be considered a potential biomarker of renal disease. We carried out a systematic review to which we included studies on HIF‐1α and renal disease in the last 5 years (2013‐2018) in researches with humans and/or animal model through searches in three databases: LILACS, PubMed, and SciELO by two researchers. We obtained 22 articles that discussed the relationship with HIF as inductor or protector against renal disease and no relation between HIF and renal. We observed controversies remain regarding the relation between of HIF with renal diseases; this may be related to the different intracellular pathways mediated by HIF‐1α, thereby determining differentiated cellular responses.