Renal oxygenation and haemodynamics in acute kidney injury and chronic kidney disease
P Singh, SE Ricksten, G Bragadottir… - Clinical and …, 2013 - Wiley Online Library
Acute kidney injury (AKI) is a major burden on health systems and may arise from multiple
initiating insults, including ischaemia‐reperfusion injury, cardiovascular surgery …
initiating insults, including ischaemia‐reperfusion injury, cardiovascular surgery …
Renoprotective approaches and strategies in acute kidney injury
Y Yang, M Song, Y Liu, H Liu, L Sun, Y Peng… - Pharmacology & …, 2016 - Elsevier
Acute kidney injury (AKI) is a major renal disease associated with high mortality rate and
increasing prevalence. Decades of research have suggested numerous chemical and …
increasing prevalence. Decades of research have suggested numerous chemical and …
Telmisartan ameliorates cisplatin-induced nephrotoxicity by inhibiting MAPK mediated inflammation and apoptosis
Nephrotoxicity is a major adverse effect of the widely used anticancer drug cisplatin.
Oxidative stress, inflammation and apoptosis are implicated in the pathophysiology of …
Oxidative stress, inflammation and apoptosis are implicated in the pathophysiology of …
Azilsartan modulates HMGB1/NF-κB/p38/ERK1/2/JNK and apoptosis pathways during renal ischemia reperfusion injury
Renal ischemia/reperfusion (IR) injury is characterized by an unexpected impairment of
blood flow to the kidney. Azilsartan is an angiotensin receptor blocker that is approved for …
blood flow to the kidney. Azilsartan is an angiotensin receptor blocker that is approved for …
Acute kidney injury after cardiac arrest
AIM: Cardiac arrest (CA) in humans causes warm renal ischemia-reperfusion injury, similar
to animal models of ischemic acute kidney injury (AKI). We aimed to investigate the …
to animal models of ischemic acute kidney injury (AKI). We aimed to investigate the …
[HTML][HTML] Angiotensin II type 1 receptor antagonists in animal models of vascular, cardiac, metabolic and renal disease
MC Michel, HR Brunner, C Foster, Y Huo - Pharmacology & therapeutics, 2016 - Elsevier
We have reviewed the effects of angiotensin II type 1 receptor antagonists (ARBs) in various
animal models of hypertension, atherosclerosis, cardiac function, hypertrophy and fibrosis …
animal models of hypertension, atherosclerosis, cardiac function, hypertrophy and fibrosis …
Xanthenone, ACE2 activator, counteracted gentamicin-induced nephrotoxicity in rats: impact on oxidative stress and ACE2/Ang-(1–7) signaling
Nephrotoxicity is a rapid deterioration of kidney function due to exposure to nephrotoxic
drugs as gentamicin. Gentamicin increases the generation of reactive oxygen species (ROS) …
drugs as gentamicin. Gentamicin increases the generation of reactive oxygen species (ROS) …
Effect of captopril treatment on recuperation from ischemia/reperfusion-induced acute renal injury
S Efrati, S Berman, RA Hamad… - Nephrology Dialysis …, 2012 - academic.oup.com
Background. Ischemia/reperfusion triggers acute kidney injury (AKI), mainly via aggravating
hypoxia, oxidative stress, inflammation and renin–angiotensin system (RAS) activation. We …
hypoxia, oxidative stress, inflammation and renin–angiotensin system (RAS) activation. We …
Reactive oxygen and nitrogen species in the renal ischemia/reperfusion injury
F Rodriguez, B Bonacasa, FJ Fenoy… - Current …, 2013 - ingentaconnect.com
Renal ischemia is the most common cause of acute kidney injury (AKI) still associated with
high mortality rates of about 50% in the intensive care unit. Postischemic AKI is …
high mortality rates of about 50% in the intensive care unit. Postischemic AKI is …
Telmisartan ameliorates nephropathy and restores the hippo pathway in rats with metabolic syndrome
B Mohamed, SA Ghareib, AE Alsemeh… - European Journal of …, 2024 - Elsevier
The main objective of this study was to determine if the telmisartan-ameliorative effects of
metabolic syndrome (MetS)-evoked nephropathy are attributed to the Hippo pathway. A …
metabolic syndrome (MetS)-evoked nephropathy are attributed to the Hippo pathway. A …