scholarly journals The role of A-kinase anchoring proteins in cardiac oxidative stress

2019 ◽  
Vol 47 (5) ◽  
pp. 1341-1353 ◽  
Author(s):  
Dario Diviani ◽  
Halima Osman ◽  
Marion Delaunay ◽  
Simon Kaiser
Keyword(s):  
Oxidative Stress ◽  
Cardiac Cells ◽  
Scaffolding Proteins ◽  
Cardiac Damage ◽  
Spatiotemporal Regulation ◽  
Anchoring Proteins ◽  
Main Driver ◽  
Dependent Protein ◽  
Detrimental Impact

Abstract Cardiac stress initiates a pathological remodeling process that is associated with cardiomyocyte loss and fibrosis that ultimately leads to heart failure. In the injured heart, a pathologically elevated synthesis of reactive oxygen species (ROS) is the main driver of oxidative stress and consequent cardiomyocyte dysfunction and death. In this context, the cAMP-dependent protein kinase (PKA) plays a central role in regulating signaling pathways that protect the heart against ROS-induced cardiac damage. In cardiac cells, spatiotemporal regulation of PKA activity is controlled by A-kinase anchoring proteins (AKAPs). This family of scaffolding proteins tether PKA and other transduction enzymes at subcellular microdomains where they can co-ordinate cellular responses regulating oxidative stress. In this review, we will discuss recent literature illustrating the role of PKA and AKAPs in modulating the detrimental impact of ROS production on cardiac function.

Naringenin improves mitochondrial function and reduces cardiac damage following ischemia-reperfusion injury: the role of the AMPK-SIRT3 signaling pathway

2019 ◽  
Vol 10 (5) ◽  
pp. 2752-2765 ◽  
Author(s):  
Li-Ming Yu ◽  
Xue Dong ◽  
Xiao-Dong Xue ◽  
Jian Zhang ◽  
Zhi Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Damage ◽  
Mitochondrial Oxidative Stress ◽  
Stress Damage

Naringenin directly inhibits mitochondrial oxidative stress damage and preserves mitochondrial biogenesisviaAMPK-SIRT3 signaling, thus attenuating MI/R injury.

1094 CHOLESTASIS INDUCES APOPTOSIS IN MICE CARDIAC CELLS: THE POSSIBLE ROLE OF NO AND OXIDATIVE STRESS

2010 ◽  
Vol 52 ◽  
pp. S423
Author(s):  
H. Shafaroodi ◽  
F. Ebrahimi ◽  
L. Moezi ◽  
M. Hashemi ◽  
Y. Doostar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Cells ◽  
And Oxidative Stress

Melatonin as a prospective metabolic regulator in pathologically altered cardiac energy homeostasis

2021 ◽  
Vol 4 (2) ◽  
pp. 316-335
Author(s):  
Swaimanti Sarkar ◽  
Aindrila Chattopadhyay ◽  
Debasish Bandyopadhyay
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion Injury ◽  
Energy Requirement ◽  
Ischemia Reperfusion ◽  
Cardiac Cells ◽  
Acid Oxidation ◽  
Ros Generation ◽  
Atp Production ◽  
Working Heart

A constant energy supply is indispensable for the relentlessly working heart. The unique metabolic flexibility of the cardiac tissue enables it to maintain its energy requirement under variable physiological conditions. However, some physiopathological statuses including aging, ischemia-reperfusion injury, diabetic cardiomyopathy, pathological cardiac hypertrophy, and heart failure frequently cause cardiac dysfunction and detrimental metabolic alteration. If the ATP supply fails to match the requirement of a working heart, the heart loses its functional capacity, resulting in slower recovery. A decrease in energy generation is often the ramifications of myocardial mitochondrial dysfunction and oxidative stress. Melatonin, a broad-spectrum antioxidant molecule has an appreciable role in the maintenance of metabolic homeostasis― from a single cell to an entire organism. Melatonin has the capacity to reduce ROS generation, preserve mitochondrial stability, and restore a robust mitochondrial function for unabated ATP production in cardiac tissues. Additionally, melatonin can promote carbohydrate and fat metabolism to further improve the ATP production in heart. In cardiac cells, melatonin upregulates GLUT4 expression either by impeding oxidative stress or by enhancing AMPK activation which accelerates fatty acid oxidation by upregulating PPAR-α and CPT-1α. Melatonin plays a pivotal role in the maintenance of calcium homeostasis in cardiomyocytes by obviating oxidative stress-mediated disruption of SERCA and NCX proteins. A possible role of melatonin to convert the Warburg effect to oxidative metabolism in pathological cardiac events has been recently contemplated. The current review will discuss the possible role of melatonin protecting against cardiac metabolic imbalances under pathological states.

Cholestasis induces apoptosis in mice cardiac cells: the possible role of nitric oxide and oxidative stress

2010 ◽  
Vol 30 (6) ◽  
pp. 898-905 ◽  
Author(s):  
Hamed Shafaroodi ◽  
Farzad Ebrahimi ◽  
Leila Moezi ◽  
Mehrdad Hashemi ◽  
Yousef Doostar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cardiac Cells ◽  
And Oxidative Stress

scholarly journals Oxidative Stress Response Is Mediated by Overexpression and Spatiotemporal Regulation of Caveolin-1

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 766
Author(s):  
Andreas Goutas ◽  
Ioanna Papathanasiou ◽  
Evanthia Mourmoura ◽  
Konstantinos Tsesmelis ◽  
Aspasia Tsezou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Dna Lesions ◽  
Damage Analysis ◽  
Structural Protein ◽  
Healthy Individuals ◽  
Caveolin 1 ◽  
Spatiotemporal Regulation ◽  
Oa Chondrocytes

Oxidative stress (OS) has been linked to the aetiology of many diseases including osteoarthritis (OA). Recent studies have shown that caveolin-1—a structural protein of plasma membrane’s caveolae—is upregulated in response to OS. Here, we explore the function of caveolin-1 in chondrocytes derived from healthy individuals (control) and OA patients that were subjected to exogenous OS. We showed that caveolin-1 was upregulated in response to acute OS in the control, but not in OA chondrocytes. Moreover, OS-induced DNA damage analysis revealed that control cells started repairing the DNA lesions 6 h post-oxidative treatment, while OA cells seemed unable to restore these damages. Importantly, in the control cells, we observed a translocation of caveolin-1 from the membrane/cytoplasm in and out of the nucleus, which coincided with the appearance and restoration of DNA lesions. When caveolin-1 was prevented from translocating to the nucleus, the control cells were unable to repair DNA damage. In OA cells, no such translocation of caveolin-1 was observed, which could account for their inability to repair DNA damage. Taken together, these results provide novel insights considering the role of caveolin-1 in response to OS-induced DNA damage while revealing its implication in the pathophysiology of OA.

scholarly journals Advances in Cardiotoxicity Induced by Altered Mitochondrial Dynamics and Mitophagy

2021 ◽  
Vol 8 ◽  
Author(s):  
Yiyuan Yin ◽  
Haitao Shen
Keyword(s):  
Energy Supply ◽  
Mitochondrial Dynamics ◽  
Cardiac Cells ◽  
Toxic Substances ◽  
Cardiac Damage ◽  
Prevention And Treatment ◽  
Underlying Mechanisms ◽  
The Stability ◽  
Normal Cardiac Function

Mitochondria are the most abundant organelles in cardiac cells, and are essential to maintain the normal cardiac function, which requires mitochondrial dynamics and mitophagy to ensure the stability of mitochondrial quantity and quality. When mitochondria are affected by continuous injury factors, the balance between mitochondrial dynamics and mitophagy is broken. Aging and damaged mitochondria cannot be completely removed in cardiac cells, resulting in energy supply disorder and accumulation of toxic substances in cardiac cells, resulting in cardiac damage and cardiotoxicity. This paper summarizes the specific underlying mechanisms by which various adverse factors interfere with mitochondrial dynamics and mitophagy to produce cardiotoxicity and emphasizes the crucial role of oxidative stress in mitophagy. This review aims to provide fresh ideas for the prevention and treatment of cardiotoxicity induced by altered mitochondrial dynamics and mitophagy.

Peptides for disruption of PKA anchoring

2006 ◽  
Vol 34 (4) ◽  
pp. 472-473 ◽  
Author(s):  
C. Hundsrucker ◽  
W. Rosenthal ◽  
E. Klussmann
Keyword(s):  
Protein Interactions ◽  
Cardiac Myocyte ◽  
Collecting Duct ◽  
Scaffolding Proteins ◽  
Protein Protein Interactions ◽  
Signalling Molecules ◽  
Cellular Processes ◽  
Anchoring Proteins ◽  
Dependent Protein ◽  
Myocyte Contractility

Adaptor or scaffolding proteins are at the basis of multiprotein complexes that spatially and temporally co-ordinate the propagation and integration of a broad range of cellular events. One class of scaffolding proteins are AKAPs (A-kinase-anchoring proteins). They sequester PKA (protein kinase A) and other signalling molecules including phosphodiesterases, other protein kinases and protein phosphatases to specific subcellular compartments. AKAP-dependent protein–protein interactions play a role in many physiologically relevant processes. For example, AKAP–PKA interactions are essential for the vasopressin-mediated water re-absorption in renal collecting duct principal cells or β-adrenoceptor-induced increases in cardiac myocyte contractility. Here, we discuss recently developed peptide disruptors of AKAP–PKA interactions. Such peptides are valuable tools to study the relevance of PKA anchoring in cellular processes.

scholarly journals High fructose and streptozotocin induced diabetic impairments are mitigated by Indirubin-3-hydrazone via downregulation of PKR pathway in Wistar rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mary Priyanka Udumula ◽  
Sureshbabu Mangali ◽  
Jaspreet Kalra ◽  
Deepika Dasari ◽  
Srashti Goyal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Jnk Pathway ◽  
Downstream Effectors ◽  
High Fructose ◽  
Dependent Protein ◽  
Metabolic Dysfunctions ◽  
Sirius Red

AbstractMetabolic disorders are becoming more common in young population due to increased consumption of carbohydrate rich diet, lack of physical activity and stress. Fructose is used as a sweetener in many carbonated beverages and is a known inducer of oxidative stress and hypertension. Up-regulation of the double-stranded RNA-dependent protein kinase (PKR) causes impairment in insulin signaling pathway and metabolic dysfunctions in type 2 diabetes mellitus. In the present study we investigated the role of PKR and associated pathways in high fructose (HF) and streptozotocin (STZ) induced diabetes and whether indirubin-3-hydrazone (IHZ), a novel PKR inhibitor can reverse the HF and STZ induced diabetic impairments in Wistar rats. Diabetes was induced by feeding rats 20% high fructose in drinking water for 6 weeks and by giving a single dose of STZ (35 mg/kg., i.p) at the end of week 5. Glucose and lipid levels were measured by using assay kits. Expression of PKR and its downstream genes were determined by immunohistochemistry, qRT-PCR and western blotting techniques. Histo-pathological studies were performed using H&E staining. Fibrosis was detected in insulin sensitive tissues and organs using Sirius red and Masson’s trichrome staining and apoptosis by TUNEL assay. HF and STZ induced hyperglycemia, fibrosis, oxidative stress, and inflammation in liver, pancreas, skeletal muscle and adipose tissue are mediated via PKR pathway and its downstream effectors, and these effects were attenuated by PKR inhibitor IHZ. Thus, inhibition of PKR can protect insulin sensitive organs and tissues from HF induced diabetic impairments via the inhibition of c-Jun N-terminal kinase (JNK) pathway.

scholarly journals The role of miR-711 in cardiac cells in response to oxidative stress and its biogenesis: a study on H9C2 cells

2020 ◽  
Vol 25 (1) ◽  
Author(s):  
Duo Zhao ◽  
Hao Zheng ◽  
Adam Greasley ◽  
Fengjun Ling ◽  
Qinfeng Zhou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Cells ◽  
H9c2 Cells
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