scholarly journals Overexpression of miR‐19a and miR‐20a in iPS‐MSCs preserves renal function of chronic kidney disease with acute ischaemia‐reperfusion injury in rat

2021 ◽  
Author(s):  
Mel S. Lee ◽  
Hon‐Kan Yip ◽  
Chih‐Chao Yang ◽  
John Y. Chiang ◽  
Tien‐Hung Huang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Renal Function ◽  
Kidney Disease ◽  
Reperfusion Injury ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Ischaemia Reperfusion

scholarly journals Effects of mycophenolate mofetil on acute ischaemia-reperfusion injury in rats and its consequences in the long term

2009 ◽  
Vol 25 (5) ◽  
pp. 1443-1450 ◽  
Author(s):  
M. Sabbatini ◽  
F. Uccello ◽  
V. Serio ◽  
G. Troncone ◽  
V. Varone ◽  
...  
Keyword(s):  
Mycophenolate Mofetil ◽  
Reperfusion Injury ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Ischaemia Reperfusion

An Introduction to Cardioprotection

2011 ◽  
Keyword(s):  
Reperfusion Injury ◽  
Myocardial Injury ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Myocardial Damage ◽  
Myocardial Salvage ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Ischaemia Reperfusion ◽  
Considerable Morbidity

• In its broadest sense, the term ‘cardioprotection’ encompasses ‘all mechanisms and means that contribute to the preservation of the heart by reducing or even preventing myocardial damage’• However, for the purposes of this book, the term ‘cardioprotection’ will refer to the endogenous mechanisms and therapeutic strategies that reduce or prevent myocardial damage induced by acute ischaemia-reperfusion injury• In this context, cardioprotection begins with the primary prevention of coronary heart disease and includes the reduction of myocardial injury sustained during coronary artery bypass graft surgery, and an acute myocardial infarction, conditions with considerable morbidity and mortality• An understanding of the pathophysiology of acute myocardial ischaemia-reperfusion injury is essential when designing new cardioprotective strategies• Several methods exist for both quantifying myocardial damage induced by acute ischaemia-reperfusion injury and for assessing myocardial salvage following the application of cardioprotective strategies• Importantly, novel cardioprotective strategies must be capable of preventing and reducing myocardial damage over and above that provided by current optimal therapy.

scholarly journals e0141 The effects and mechanisms between DIDS and EDRV on acute ischaemia-reperfusion injury myocardium

Heart ◽  
2010 ◽  
Vol 96 (Suppl 3) ◽  
pp. A45-A45
Author(s):  
L. Yan-xia ◽  
L. Jia-ni ◽  
S. Ming-zhi ◽  
Z. Meng ◽  
Z. Ya-li ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Ischaemia Reperfusion

Akt protects the heart against ischaemia-reperfusion injury by modulating mitochondrial morphology

2015 ◽  
Vol 113 (03) ◽  
pp. 513-521 ◽  
Author(s):  
Sang-Bing Ong ◽  
Andrew Hall ◽  
Rachel Dongworth ◽  
Siavash Kalkhoran ◽  
Aswin Pyakurel ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Mitochondrial Permeability Transition ◽  
Cardiac Cells ◽  
Mitochondrial Morphology ◽  
Myocardial Infarct Size ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Mptp Opening ◽  
Ischaemia Reperfusion ◽  
Mitochondrial Elongation

SummaryThe mechanism through which the protein kinase Akt (also called PKB), protects the heart against acute ischaemia-reperfusion injury (IRI) is not clear. Here, we investigate whether Akt mediates its cardioprotective effect by modulating mitochondrial morphology. Transfection of HL-1 cardiac cells with constitutively active Akt (caAkt) changed mitochondrial morphology as evidenced by an increase in the proportion of cells displaying predominantly elongated mitochondria (73 ± 5.0 % caAkt vs 49 ± 5.8 % control: N=80 cells/group; p< 0.05). This effect was associated with delayed time taken to induce mitochondrial permeability transition pore (MPTP) opening (by 2.4 ± 0.5 fold; N=80 cells/group: p< 0.05); and reduced cell death following simulated IRI (32.8 ± 1.2 % caAkt vs 63.8 ± 5.6 % control: N=320 cells/group: p< 0.05). Similar effects on mitochondrial morphology, MPTP opening, and cell survival post-IRI, were demonstrated with pharmacological activation of Akt using the known cardioprotective cytokine, erythropoietin (EPO). The effect of Akt on inducing mitochondrial elongation was found to be dependent on the mitochondrial fusion protein, Mitofusin-1 (Mfn1), as ablation of Mfn1 in mouse embryonic fibroblasts (MEFs) abrogated Akt-mediated mitochondrial elongation. Finally, in vivo pre-treatment with EPO reduced myocardial infarct size (as a % of the area at risk) in adult mice subjected to IRI (26.2 ± 2.6 % with EPO vs 46.1 ± 6.5 % in control; N=7/group: p< 0.05), and reduced the proportion of cells displaying myofibrillar disarray and mitochondrial fragmentation observed by electron microscopy in adult murine hearts subjected to ischaemia from 5.8 ± 1.0 % to 2.2 ± 1.0 % (N=5 hearts/group; p< 0.05). In conclusion, we found that either genetic or pharmacological activation of Akt protected the heart against acute ischaemia-reperfusion injury by modulating mitochondrial morphology.

scholarly journals Sustained Isoprostane E2 Elevation, Inflammation and Fibrosis after Acute Ischaemia-Reperfusion Injury Are Reduced by Pregnane X Receptor Activation

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0136173 ◽  
Author(s):  
Aimen O. Amer ◽  
Philip M. Probert ◽  
Michael Dunn ◽  
Margaret Knight ◽  
Abigail E. Vallance ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Pregnane X Receptor ◽  
Receptor Activation ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Ischaemia Reperfusion

scholarly journals Murine models of renal ischaemia reperfusion injury: An opportunity for refinement using non-invasive monitoring methods

2019 ◽  
Author(s):  
Rachel Harwood ◽  
Joshua Bridge ◽  
Lorenzo Ressel ◽  
Lauren Scarfe ◽  
Jack Sharkey ◽  
...  
Keyword(s):  
Renal Function ◽  
Reperfusion Injury ◽  
Kidney Function ◽  
Kidney Injury ◽  
Ischaemia Reperfusion Injury ◽  
Optoacoustic Tomography ◽  
Non Invasive ◽  
Renal Ischaemia ◽  
Ischaemia Reperfusion

BackgroundRenal Ischaemia Reperfusion Injury (R-IRI) can cause Acute Kidney Injury (AKI) and Chronic Kidney Disease (CKD), resulting in significant morbidity and mortality. To understand the underlying mechanisms, reproducible small-animal models of AKI and CKD are needed. We describe how innovative technologies for measuring kidney function non-invasively in small rodents allow successful refinement of the R-IRI models, and offer the unique opportunity to monitor longitudinally in individual animals the transition from AKI to CKD.MethodsMale BALB/c mice underwent bilateral renal pedicle clamping (AKI) or unilateral renal pedicle clamping with delayed contralateral nephrectomy (CKD) under isoflurane anaesthetic. Transdermal GFR monitoring and multi-spectral optoacoustic tomography in combination with statistical analysis were used to identify and standardise variables within these models.ResultsPre-clamping anaesthetic time was one of the most important predictors of AKI severity after R-IRI. Standardising pre-clamping time resulted in a more predictably severe AKI model. In the CKD model, initial improvement in renal function was followed by significant progressive reduction in function between weeks 2 and 4. Performing contralateral nephrectomy on day 14 enabled the development of CKD in a survivable way.ConclusionsNon-invasive monitoring of global and individual renal function after R-IRI is feasible, reproducible and correlates well with classical markers of injury. This facilitates refinement of kidney injury models and enables the degree of injury seen in pre-clinical models to be translated to those seen in the clinical setting. Thus, future therapies can be tested in a clinically relevant, non-invasive manner.What is already knownThe severity of Renal Ischaemia Reperfusion injury (R-IRI) varies between animal strain, gender and age. Experimental variables including temperature and clamping time are usually tightly controlled but significant variability still exists. Classically, small rodent experiments depend on endpoint evaluation of serum and histological features of disease. However, new technologies including transdermal glomerular filtration rate (GFR) monitoring and Multispectral Optoacoustic Tomography (MSOT) may enable renal function to be accurately monitored longitudinally, enabling better refinement of these models.What this study addsThis study shows that transdermal GFR measurements have reliably enabled refinement of the R-IRI model by standardisation of the duration of isoflurane prior to commencing surgery. Individual kidney function can be assessed in-vivo after unilateral R-IRI using MSOT imaging. The excretion tmax of IRDye-800 reliably represents the relative function of the injured kidney, permitting longitudinal in-vivo assessment of differential kidney function.What impact this may have on practiceThis study demonstrates the utility of two minimally-invasive in-vivo methods of monitoring kidney function which have advantages over classical methods and potentially enable fewer animals to be used in future studies. The study demonstrates refinement of bilateral and unilateral R-IRI models which will also enable a reduction in the number of animals needed for experimentation.

Activated protein C attenuates acute ischaemia reperfusion injury in skeletal muscle

2005 ◽  
Vol 23 (6) ◽  
pp. 1454-1459 ◽  
Author(s):  
J DILLON ◽  
A LAING ◽  
R CAHILL ◽  
G OBRIEN ◽  
J STREET ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Reperfusion Injury ◽  
Protein C ◽  
Activated Protein C ◽  
Ischaemia Reperfusion Injury ◽  
Acute Ischaemia ◽  
Ischaemia Reperfusion
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