2018
DOI: 10.1016/j.nefro.2017.11.013
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The use of cell cycle arrest biomarkers in the early detection of acute kidney injury. Is this the new renal troponin?

Abstract: Acute kidney injury (AKI) has a high prevalence in critical care patients. Early detection might prevent patients from developing chronic kidney disease and requirement for renal replacement therapy. If we compare AKI with acute coronary syndrome, in which an increase in cardiac troponin may trigger early diagnosis and therapeutic intervention, we could extrapolate a similar technique in patients with early AKI without changes in urinary frequency or serum creatinine. The objective is to identify biomarker-pos… Show more

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Cited by 28 publications
(18 citation statements)
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“…During renal injury in the early phases of AKI, several tumor suppressor proteins like p53, p27 and p21 can be activated, and they upregulate different proteins. 11 IGFBP-7 directly increases the expression of p53 and p21, while TIMP-2 enhances p27 expression. These effects are carried in an autocrine and paracrine pattern through IGFBP-7 and TIMP-2 receptors.…”
Section: Tissue Inhibitor Of Metalloproteinase 2 (Timp-2) and Insulinmentioning
confidence: 91%
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“…During renal injury in the early phases of AKI, several tumor suppressor proteins like p53, p27 and p21 can be activated, and they upregulate different proteins. 11 IGFBP-7 directly increases the expression of p53 and p21, while TIMP-2 enhances p27 expression. These effects are carried in an autocrine and paracrine pattern through IGFBP-7 and TIMP-2 receptors.…”
Section: Tissue Inhibitor Of Metalloproteinase 2 (Timp-2) and Insulinmentioning
confidence: 91%
“…Some authors postulated that these proteins cause cell-cycle arrest during the very early phase of cellular damage leading the cell-cycle arrest in G1 phase in response to various insults (eg oxidative stress, toxins, ischemia, sepsis, inflammation). 11,12 Cells react to injury by repairing while entering and exiting different phases of proliferation assisted by kinases. G1 cell-cycle arrest prevents division of cells with damaged DNA, allowing an adequate repair ( Figure 1).…”
Section: Tissue Inhibitor Of Metalloproteinase 2 (Timp-2) and Insulinmentioning
confidence: 99%
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“…TIMP-2 has a molecular weight of approximately 24 kDa and IGFBP7 has a molecular mass of 29 kDa [ 110 ]. Both of them are expressed and secreted by renal tubular cells, and involved in G1 cell cycle arrest during the early phases of cellular stress or injury caused by various insults (e.g., sepsis, ischemia, oxidative stress, and toxins) [ 111 ]. TIMP-2/ IGFBP7 shows the best accuracy among AKI biomarkers in patients with various types of AKI condition including AKI after kidney transplantation and AKI in critical care settings, sepsis and platinum-based chemotherapy, and chronic kidney damage induced by diabetes mellitus and congestive heart failure [ 112 , 113 ].…”
Section: Biomarkers Of Uutomentioning
confidence: 99%
“…TIMP-2 and IGFBP-7 are expressed and secreted in the kidneys as well as other tissues. Some authors postulated that these proteins halt the G1 phase of the cell cycle in response to different factors (for example, oxidative stress, toxins, ischemia, sepsis, and in lammation); their signaling pathways also have an autocrine and paracrine pattern [51,52]. Hence, markers of cellular cycle detention like TIMP-2 and IGFBP-7 act as a warning sign that tubular cells have been a subject of stress and have to shut down their function to preserve energy.…”
Section: Nephrocheckmentioning
confidence: 99%