Kinetics of the Cell Cycle Arrest Biomarkers TIMP2 and IGFBP7 for the Biology Diagrams Sepsis-associated acute kidney injury (SA-AKI) is a severe complication in critically ill patients, with a complex pathogenesis involving in cell cycle arrest, microcirculatory dysfunction, and inflammation. Current diagnostic strategies remain suboptimal. Therefore, this study aimed to evaluate pat โฆ
Derivation and validation of cutoffs for clinical use of cell cycle arrest biomarkers Nephrol Dial Transplant. 2014 Nov;29(11) :2054-61. metalloproteinases (TIMP)-2 and insulin-like growth factor binding protein (IGFBP)7 are two recently discovered urinary biomarkers for AKI. We now report on the development, and diagnostic accuracy of two
Cell Cycle Arrest Biomarkers in the Intensive Care Unit Biology Diagrams
The cell cycle arrest markers tissue inhibitor metalloproteinases-2 (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP7) have been identified as potential biomarkers of acute kidney In a biomarker-based approach, these two G1 cell cycle arrest markers guided the implementation of a bundle of supportive measures which was associated with a significantly reduced occurrence of AKI . Such a patient individualized approach using novel biomarkers could also be beneficial for COVID-19 patients in order to improve outcomes.
TIMP-2 and IGFBP-7 are identified as effective biomarkers for cell cycle arrest during the progression of AKI. Ang-2 has a great contribution to microvascular dysfunction in sepsis. The cell cycle biomarkers have been shown to be involved in a diverse array of biologic processes, including cell cycle arrest. In the setting of cell cycle arrest, these proteins signal activation of the p-protein cascade (p53, p21 and p27), which in turn blocks the effect of the cyclin-dependent protein kinase complexes [28- 32]. The two top biomarkers from discovery were validated. Urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2), both inducers of G1 cell cycle arrest, a key mechanism implicated in AKI, together demonstrated an AUC of 0.80 (0.76 and 0.79 alone).
Biomarkers of cell cycle arrest, microcirculation dysfunction, and ... Biology Diagrams
The two top biomarkers from discovery were validated. Urine insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP-2), both inducers of G1 cell cycle arrest, a key mechanism implicated in AKI, together demonstrated an AUC of 0.80 (0.76 and 0.79 alone). Cell cycle arrest biomarkers, TIMP-2 and IGFBP7, improve risk stratification for severe outcomes in patients with stage 1 acute kidney injury by urine output, serum creatinine or both, with risk increasing with each acute kidney injury indicator. Longer term outcomes demonstrate that the associated risks of a [TIMP-2]โข[IGFBP7] greater than 2.
