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Basic Research in Cardiology

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https://www.readbyqxmd.com/read/29392420/cardioprotective-effect-of-ghrelin-against-myocardial-infarction-induced-left-ventricular-injury-via-inhibition-of-socs3-and-activation-of-jak2-stat3-signaling
#1
Refaat A Eid, Mahmoud A Alkhateeb, Samy Eleawa, Fahaid H Al-Hashem, Mubarak Al-Shraim, Attalla Farag El-Kott, Mohamed Samir Ahmed Zaki, Mohammad A Dallak, Hussain Aldera
The molecular mechanisms through which ghrelin exerts its cardioprotective effects during cardiac remodeling post-myocardial infarction (MI) are poorly understood. The aim of this study was to investigate whether the cardioprotection mechanisms are mediated by modulation of JAK/STAT signaling and what triggers this modulation. Rats were divided into six groups (n = 12/group): control, sham, sham + ghrelin (100 µg/kg, s.c., daily, starting 1 day post-MI), MI, MI+ ghrelin, and MI+ ghrelin+ AG490, a potent JAK2 inhibitor (5 mg/kg, i...
February 1, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29349588/amphiregulin-enhances-cardiac-fibrosis-and-aggravates-cardiac-dysfunction-in-mice-with-experimental-myocardial-infarction-partly-through-activating-egfr-dependent-pathway
#2
Liang Liu, Xian Jin, Cui-Fen Hu, Ya-Ping Zhang, Zhong'e Zhou, Rong Li, Cheng-Xing Shen
Cardiac fibrosis (CF), a main process of ventricular remodeling after myocardial infarction (MI), plays a crucial role in the pathogenesis of heart failure (HF) post-MI. It is known that amphiregulin (AR) is involved in fibrosis of several organs. However, the expression of AR and its role post-MI are yet to be determined. This study aimed to investigate the impact of AR on CF post-MI and related mechanisms. Significantly upregulated AR expression was evidenced in the infarct border zone of MI mice in vivo and the AR secretion was enhanced in macrophages, but not in cardiac fibroblasts...
January 18, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29344827/molecular-imaging-of-cardiac-remodelling-after-myocardial-infarction
#3
REVIEW
Daniel Curley, Begoña Lavin Plaza, Ajay M Shah, René M Botnar
Myocardial infarction and subsequent heart failure is a major health burden associated with significant mortality and morbidity in western societies. The ability of cardiac tissue to recover after myocardial infarction is affected by numerous complex cellular and molecular pathways. Unbalance or failure of these pathways can lead to adverse remodelling of the heart and poor prognosis. Current clinical cardiac imaging modalities assess anatomy, perfusion, function, and viability of the myocardium, yet do not offer any insight into the specific molecular pathways involved in the repair process...
January 17, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29344719/phosphorylation-of-vasodilator-stimulated-phosphoprotein-contributes-to-myocardial-ischemic-preconditioning
#4
David Köhler, Sofia-Iris Bibli, Lothar P Klammer, Judith M Roth, Rainer Lehmann, Ingrid Fleming, Tiago F Granja, Andreas Straub, Peter M Benz, Peter Rosenberger
Ischemic preconditioning (IP) is a well-known strategy to protect organs against cell death following ischemia. The previous work has shown that vasodilator-stimulated phosphoprotein (VASP) is involved in cytoskeletal reorganization and that it holds significant importance for the extent of myocardial ischemia reperfusion injury. Yet, the role of VASP during myocardial IP is, to date, not known. We report here that VASP phosphorylation at serine157 and serine239 is induced during hypoxia in vitro and during IP in vivo...
January 17, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29335904/the-safe-pathway-for-cardioprotection-is-this-a-promising-target
#5
REVIEW
Nkanyiso Hadebe, Martin Cour, Sandrine Lecour
The survivor activating factor enhancement (SAFE) pathway was discovered as an alternative intrinsic pro-survival signaling pathway to the reperfusion injury salvage kinase pathway for cardioprotection against ischemia-reperfusion injury. The delineation of this pathway, made of key components such as cytokines of the immune system and transcription factors, has brought major advancements in our understanding on how the heart is able to protect itself against ischemia-reperfusion injury. In this viewpoint, we describe the major steps leading to the discovery of the SAFE pathway in small animal models to date and we discuss its translation to large animals and humans...
January 15, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29288409/gene-expression-analysis-to-identify-mechanisms-underlying-heart-failure-susceptibility-in-mice-and-humans
#6
Christoph Koentges, Mark E Pepin, Carolyn Müsse, Katharina Pfeil, Sonia V Viteri Alvarez, Natalie Hoppe, Michael M Hoffmann, Katja E Odening, Samuel Sossalla, Andreas Zirlik, Lutz Hein, Christoph Bode, Adam R Wende, Heiko Bugger
Genetic factors are known to modulate cardiac susceptibility to ventricular hypertrophy and failure. To determine how strain influences the transcriptional response to pressure overload-induced heart failure (HF) and which of these changes accurately reflect the human disease, we analyzed the myocardial transcriptional profile of mouse strains with high (C57BL/6J) and low (129S1/SvImJ) susceptibility for HF development, which we compared to that of human failing hearts. Following transverse aortic constriction (TAC), C57BL/6J mice developed overt HF while 129S1/SvImJ did not...
December 29, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29273902/ampk-dependent-nitric-oxide-release-provides-contractile-support-during-hyperosmotic-stress
#7
Malena Morell, Juan Ignacio Burgos, Luis Alberto Gonano, Martin Vila Petroff
In different pathological situations, cardiac cells undergo hyperosmotic stress (HS) and cell shrinkage. This change in cellular volume has been associated with contractile dysfunction and cell death. Given that nitric oxide (NO) is a well-recognized modulator of cardiac contractility and cell survival, we evaluated whether HS increases NO production and its impact on the negative inotropic effect observed during this type of stress. Superfusing cardiac myocytes with a hypertonic solution (HS: 440 mOsm) decreased cell volume and increased NO-sensitive DAF-FM fluorescence compared with myocytes superfused with an isotonic solution (IS: 309 mOsm)...
December 22, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29242986/pre-and-postconditioning-the-heart-with-hydrogen-sulfide-h2s-against-ischemia-reperfusion-injury-in-vivo-a-systematic-review-and-meta-analysis
#8
REVIEW
Qutuba G Karwi, Justin S Bice, Gary F Baxter
Conditioning-like infarct limitation by enhanced level of hydrogen sulfide (H2S) has been demonstrated in many animal models of myocardial ischemia/reperfusion injury (MIRI) in vivo. We sought to evaluate the effect of H2S on myocardial infarction across in vivo pre-clinical studies of MIRI using a comprehensive systematic review followed by meta-analysis. Embase, Pubmed and Web of Science were searched for pre-clinical investigation of the effect of H2S on MIRI in vivo. Retained records (6031) were subjected to our pre-defined inclusion criteria then were objectively critiqued...
December 14, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29224086/role-of-nlrp3-inflammasome-in-the-pathogenesis-of-cardiovascular-diseases
#9
REVIEW
Dongling Liu, Xiang Zeng, Xiao Li, Jawahar L Mehta, Xianwei Wang
NLRP3 inflammasome is a key multiprotein signaling platform that tightly controls inflammatory responses and coordinates antimicrobial host defenses by activating caspase-1 for the subsequent maturation of pro-inflammatory cytokines, IL-1β and IL-18, and induces pyroptosis. The assembly and activation of NLRP3 inflammasome are linked to the pathogenesis of several cardiovascular disease risk factors, such as hypertension and diabetes, and their major consequences-myocardial remodeling. The study of the NLRP3 inflammasome in these cardiovascular disease states may uncover important triggers and endogenous modulators of the disease, and lead to new treatment strategies...
December 9, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29164342/survival-pathways-in-cardiac-conditioning-individual-data-vs-meta-analyses-what-do-we-learn
#10
EDITORIAL
Rainer Schulz, Bence Ágg, Péter Ferdinandy
No abstract text is available yet for this article.
November 21, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29159507/stat3-as-a-common-signal-of-ischemic-conditioning-a-lesson-on-rigor-and-reproducibility-in-preclinical-studies-on-cardioprotection
#11
Petra Kleinbongard, Andreas Skyschally, Sabine Gent, Marion Pesch, Gerd Heusch
Ischemic conditioning before (ischemic preconditioning, IPC) or after (ischemic postconditioning, POCO) sustained myocardial ischemia/reperfusion (I/R), induced locally or remotely from the heart (remote IPC, RIPC), reduces infarct size. However, none of the identified signaling steps of ischemic conditioning was robust across models and species to be successfully translated to humans. In prior separate studies in pigs, activation of signal transducer and activator of transcription 3 (STAT3) was causal for infarct size reduction by IPC, POCO, and RIPC but it remains unclear whether or not STAT3 is truly a common denominator of cardioprotective signaling...
November 20, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29143177/the-risk-pathway-and-beyond
#12
REVIEW
Xavier Rossello, Derek M Yellon
Research on cardioprotection has attracted considerable attention during the past 30 years following the discovery of ischemic preconditioning with great advances being made in the field, particularly in the description of the molecular signalling behind this cardioprotective intervention. In a time when basic research is struggling to translate its findings into therapies in the clinical setting, this viewpoint has the intention of presenting to clinical and basic scientists how the reperfusion injury salvage kinase pathway has been described and dissected, as well as highlighting its relevance in cardioprotection...
November 15, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29101484/periostin-in-cardiovascular-disease-and-development-a-tale-of-two-distinct-roles
#13
REVIEW
Natalie M Landry, Smadar Cohen, Ian M C Dixon
Tissue development and homeostasis are dependent upon the concerted synthesis, maintenance, and degradation of extracellular matrix (ECM) molecules. Cardiac fibrosis is now recognized as a primary contributor to incidence of heart failure, particularly heart failure with preserved ejection fraction, wherein cardiac filling in diastole is compromised. Periostin is a cell-associated protein involved in cell fate determination, proliferation, tumorigenesis, and inflammatory responses. As a non-structural component of the ECM, secreted 90 kDa periostin is emerging as an important matricellular factor in cardiac mesenchymal tissue development...
November 3, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29079873/regenerating-the-human-heart-direct-reprogramming-strategies-and-their-current-limitations
#14
REVIEW
Andrea Ghiroldi, Marco Piccoli, Giuseppe Ciconte, Carlo Pappone, Luigi Anastasia
Cardiovascular diseases are the leading cause of death in the Western world. Unfortunately, current therapies are often only palliative, consequently essentially making heart transplantation necessary for many patients. However, several novel therapeutic approaches in the past two decades have yielded quite encouraging results. The generation of induced pluripotent stem cells, through the forced expression of stem cell-specific transcription factors, has inspired the most promising strategies for heart regeneration by direct reprogramming of cardiac fibroblasts into functional cardiomyocytes...
October 27, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29071437/effect-of-long-term-remote-ischemic-conditioning-in-patients-with-chronic-ischemic-heart-failure
#15
Kasper Pryds, Roni Ranghøj Nielsen, Anders Jorsal, Mona Sahlholdt Hansen, Steffen Ringgaard, Jens Refsgaard, Won Yong Kim, Annemette Krintel Petersen, Hans Erik Bøtker, Michael Rahbek Schmidt
Remote ischemic conditioning (RIC) protects against acute ischemia-reperfusion injury and may also have beneficial effects in patients with stable cardiovascular disease. We investigated the effect of long-term RIC treatment in patients with chronic ischaemic heart failure (CIHF). In a parallel group study, 22 patients with compensated CIHF and 21 matched control subjects without heart failure or ischemic heart disease were evaluated by cardiac magnetic resonance imaging, cardiopulmonary exercise testing, skeletal muscle function testing, blood pressure measurement and blood sampling before and after 28 ± 4 days of once daily RIC treatment...
October 25, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29043508/the-role-of-pi3k%C3%AE-isoform-in-cardioprotection
#16
Xavier Rossello, Jaime A Riquelme, Zhenhe He, Stasa Taferner, Bart Vanhaesebroeck, Sean M Davidson, Derek M Yellon
Ischemic preconditioning (IPC) limits myocardial infarct size through the activation of the PI3K-Akt signal cascade; however, little is known about the roles of individual PI3K isoforms in cardioprotection. We aimed, therefore, to elucidate the role of the PI3Kα isoform in cardioprotection Pharmacological PI3Kα inhibition was assessed in isolated-perfused mouse hearts subjected to ischemia/reperfusion injury (IRI), either during the IPC procedure or at reperfusion. PI3Kα inhibition abrogated the IPC-induced protective effect at reperfusion, but not when given only during the IPC protocol...
October 17, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28965130/regulation-of-myocardial-oxygen-delivery-in-response-to-graded-reductions-in-hematocrit-role-of-k-channels
#17
Alexander M Kiel, Adam G Goodwill, Jillian N Noblet, April L Barnard, Daniel J Sassoon, Johnathan D Tune
This study was designed to identify mechanisms responsible for coronary vasodilation in response to progressive decreases in hematocrit. Isovolemic hemodilution was produced in open-chest, anesthetized swine via concurrent removal of 500 ml of arterial blood and the addition of 500 ml of 37 °C saline or synthetic plasma expander (Hespan, 6% hetastarch in 0.9% sodium chloride). Progressive hemodilution with Hespan resulted in an increase in coronary flow from 0.39 ± 0.05 to 1.63 ± 0.16 ml/min/g (P < 0...
September 30, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28952016/the-impact-of-irreproducibility-and-competing-protection-from-p2y12-antagonists-on-the-discovery-of-cardioprotective-interventions
#18
REVIEW
Michael V Cohen, James M Downey
Scientists and clinicians have been concerned by the lack of a clinically suitable strategy for cardioprotection in patients with acute myocardial infarction despite decades of intensive pre-clinical investigations and a surprising number of clinical trials based on those observations which have uniformly been disappointing. However, it would be a mistake to abandon this search. Rather it would be useful to examine these past efforts and determine reasons for the multiple failures. It appears that earlier clinical trials were often based on results from a single experimental laboratory, thus minimizing the importance of establishing reproducibility in multiple laboratories by multiple scientists and in multiple models...
September 26, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28913715/oxidized-low-density-lipoprotein-oxldl-affects-load-free-cell-shortening-of-cardiomyocytes-in-a-proprotein-convertase-subtilisin-kexin-9-pcsk9-dependent-way
#19
Klaus-Dieter Schlüter, Annemarie Wolf, Martin Weber, Rolf Schreckenberg, Rainer Schulz
Recent studies have documented that oxidized low-density lipoprotein cholesterol (oxLDL) levels directly impact myocardial structure and function. However, the molecular mechanisms by which oxLDL affects cardiac myocytes are not well established. We addressed the question whether oxLDL modifies load-free cell shortening, a standardized readout of cardiac cellular function, and investigated whether proprotein convertase subtilisin/kexin-9 (PCSK9) is involved on oxLDL-dependent processes. Adult rat ventricular cardiomyocytes were isolated and incubated for 24 h with oxLDL...
September 14, 2017: Basic Research in Cardiology
https://www.readbyqxmd.com/read/28913553/dual-inhibition-of-cathepsin-g-and-chymase-reduces-myocyte-death-and-improves-cardiac-remodeling-after-myocardial-ischemia-reperfusion-injury
#20
Bahman Hooshdaran, Mikhail A Kolpakov, Xinji Guo, Sonni A Miller, Tao Wang, Douglas G Tilley, Khadija Rafiq, Abdelkarim Sabri
Early reperfusion of ischemic cardiac tissue increases inflammatory cell infiltration which contributes to cardiomyocyte death and loss of cardiac function, referred to as ischemia/reperfusion (IR) injury. Neutrophil- and mast cell-derived proteases, cathepsin G (Cat.G) and chymase, are released early after IR, but their function is complicated by potentially redundant actions and targets. This study investigated whether a dual inhibition of Cat.G and chymase influences cardiomyocyte injury and wound healing after experimental IR in mice...
September 14, 2017: Basic Research in Cardiology
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