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Basic Research in Cardiology

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https://www.readbyqxmd.com/read/29915952/apolipoprotein-a-i-proteolysis-in-aortic-valve-stenosis-role-of-cathepsin-s
#1
C Gebhard, F Maafi, B E Stähli, J Dang, W Nachar, A B de Oliveira Moraes, A E Kernaleguen, V Lavoie, M Mecteau, T Mihalache-Avram, Y Shi, M Chabot-Blanchet, D Busseuil, D Rhainds, E Rhéaume, Jean-Claude Tardif
Aortic valve stenosis (AVS) is the most common valvular heart disease in the Western world. Therapy based on apolipoprotein A-I (apoA-I), the major protein component of high-density lipoproteins, results in AVS regression in experimental models. Nevertheless, apoA-I degradation by proteases might lead to suboptimal efficacy of such therapy. An activatable probe using a quenched fluorescently labeled full-length apoA-I protein was generated to assess apoA-I-degrading protease activity in plasma derived from 44 men and 20 women with severe AVS (age 65...
June 18, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29905892/physiological-and-unappreciated-roles-of-camkii-in-the-heart
#2
REVIEW
Jan Beckendorf, Maarten M G van den Hoogenhof, Johannes Backs
In the cardiomyocyte, CaMKII has been identified as a nodal influencer of excitation-contraction and also excitation-transcription coupling. Its activity can be regulated in response to changes in intracellular calcium content as well as after several post-translational modifications. Some of the effects mediated by CaMKII may be considered adaptive, while effects of sustained CaMKII activity may turn into the opposite and are detrimental to cardiac integrity and function. As such, CaMKII has long been noted as a promising target for pharmacological inhibition, but the ubiquitous nature of CaMKII has made it difficult to target CaMKII specifically where it is detrimental...
June 15, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29892894/cardiomyocyte-dimethylarginine-dimethylaminohydrolase1-attenuates-left-ventricular-remodeling-after-acute-myocardial-infarction-involvement-in-oxidative-stress-and-apoptosis
#3
Lei Hou, Junjie Guo, Feng Xu, Xinyu Weng, Wenhui Yue, Junbo Ge
Asymmetric dimethylarginine (ADMA) is a risk factor for heart diseases. Dimethylarginine dimethylaminohydrolase (DDAH) enzymes are key proteins for ADMA degradation. Endothelial DDAH1 is a vital regulator of angiogenesis. DDAH1 is also expressed in cardiomyocytes. However, the role of DDAH1 in cardiomyocytes needs further clarification. Herein, we used an inducible cardiac-specific DDAH1 knockdown mouse (cardiac DDAH1-/- ) to investigate the role of cardiomyocyte DDAH1 in left-ventricular (LV) remodeling after acute myocardial infarction (AMI)...
June 11, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29881975/atrial-fibrillation-and-heart-failure-associated-remodeling-of-two-pore-domain-potassium-k-2p-channels-in-murine-disease-models-focus-on-task-1
#4
Felix Wiedmann, Jan S Schulte, Bruna Gomes, Maria-Patapia Zafeiriou, Antonius Ratte, Franziska Rathjens, Edda Fehrmann, Beatrix Scholz, Niels Voigt, Frank Ulrich Müller, Dierk Thomas, Hugo A Katus, Constanze Schmidt
Understanding molecular mechanisms involved in atrial tissue remodeling and arrhythmogenesis in atrial fibrillation (AF) is essential for developing specific therapeutic approaches. Two-pore-domain potassium (K2P ) channels modulate cellular excitability, and TASK-1 (K2P 3.1) currents were recently shown to alter atrial action potential duration in AF and heart failure (HF). Finding animal models of AF that closely resemble pathophysiological alterations in human is a challenging task. This study aimed to analyze murine cardiac expression patterns of K2P channels and to assess modulation of K2P channel expression in murine models of AF and HF...
June 7, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29868933/mapping-macrophage-polarization-over-the-myocardial-infarction-time-continuum
#5
Alan J Mouton, Kristine Y DeLeon-Pennell, Osvaldo J Rivera Gonzalez, Elizabeth R Flynn, Tom C Freeman, Jeffrey J Saucerman, Michael R Garrett, Yonggang Ma, Romain Harmancey, Merry L Lindsey
In response to myocardial infarction (MI), cardiac macrophages regulate inflammation and scar formation. We hypothesized that macrophages undergo polarization state changes over the MI time course and assessed macrophage polarization transcriptomic signatures over the first week of MI. C57BL/6 J male mice (3-6 months old) were subjected to permanent coronary artery ligation to induce MI, and macrophages were isolated from the infarct region at days 1, 3, and 7 post-MI. Day 0, no MI resident cardiac macrophages served as the negative MI control...
June 4, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29858664/neural-mechanisms-in-remote-ischaemic-conditioning-in-the-heart-and-brain-mechanistic-and-translational-aspects
#6
REVIEW
Marina V Basalay, Sean M Davidson, Andrey V Gourine, Derek M Yellon
Remote ischaemic conditioning (RIC) is a promising method of cardioprotection, with numerous clinical studies having demonstrated its ability to reduce myocardial infarct size and improve prognosis. On the other hand, there are several clinical trials, in particular those conducted in the setting of elective cardiac surgery, that have failed to show any benefit of RIC. These contradictory data indicate that there is insufficient understanding of the mechanisms underlying RIC. RIC is now known to signal indiscriminately, protecting not only the heart, but also other organs...
June 1, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29766323/cgmp-at-the-centre-of-attention-emerging-strategies-for-activating-the-cardioprotective-pkg-pathway
#7
REVIEW
Min Park, Peter Sandner, Thomas Krieg
The nitric oxide (NO)-protein kinase G (PKG) pathway has been known for some time to be an important target for cardioprotection against ischaemia/reperfusion injury and heart failure. While many approaches for reducing infarct size in patients have failed in the past, the advent of novel drugs that modulate cGMP and its downstream targets shows very promising results in recent preclinical and clinical studies. Here, we review main aspects of the NO-PKG pathway in light of recent drug development and summarise potential cardioprotective strategies in which cGMP is the main player...
May 15, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29744667/vagus-nerve-stimulation-exerts-cardioprotection-against-myocardial-ischemia-reperfusion-injury-predominantly-through-its-efferent-vagal-fibers
#8
Watthana Nuntaphum, Wanpitak Pongkan, Suwakon Wongjaikam, Savitree Thummasorn, Pongpan Tanajak, Juthamas Khamseekaew, Kannaporn Intachai, Siriporn C Chattipakorn, Nipon Chattipakorn, Krekwit Shinlapawittayatorn
Vagus nerve stimulation (VNS) has been shown to exert cardioprotection against myocardial ischemia/reperfusion (I/R) injury. However, whether the cardioprotection of VNS is mainly due to direct activation through its ipsilateral efferent fibers (motor) rather than indirect effects mediated by the afferent fibers (sensory) have not been clearly understood. We hypothesized that VNS exerts cardioprotection predominantly through its efferent vagal fibers. Thirty swine (30-35 kg) were randomized into five groups: I/R no VNS (I/R), and left mid-cervical VNS with both vagal trunks intact (LC-VNS), with left vagus nerve transection (LtVNX), with right vagus nerve transection (RtVNX) and with atropine pretreatment (Atropine), respectively...
May 9, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29744594/nr4a1-aggravates-the-cardiac-microvascular-ischemia-reperfusion-injury-through-suppressing-fundc1-mediated-mitophagy-and-promoting-mff-required-mitochondrial-fission-by-ck2%C3%AE
#9
Hao Zhou, Jin Wang, Pingjun Zhu, Hong Zhu, Sam Toan, Shunying Hu, Jun Ren, Yundai Chen
Mitochondrial fission and mitophagy are considered key processes involved in the pathogenesis of cardiac microvascular ischemia reperfusion (IR) injury although the upstream regulatory mechanism for fission and mitophagy still remains unclear. Herein, we reported that NR4A1 was significantly upregulated following cardiac microvascular IR injury, and its level was positively correlated with microvascular collapse, endothelial cellular apoptosis and mitochondrial damage. However, NR4A1-knockout mice exhibited resistance against the acute microvascular injury and mitochondrial dysfunction compared with the wild-type mice...
May 9, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29671120/retraction-note-to-compensatory-role-of-the-nbcn1-sodium-bicarbonate-cotransporter-on-ca-2-induced-mitochondrial-swelling-in-hypertrophic-hearts
#10
Lorena A Vargas, Fernanda Carrizo Velasquez, Bernardo V Alvarez
The authors have retracted this article [1] because of modifications in the control lanes of Figs. 2a and 8a of the COX1 blot obtained for 18-week-old rats (rotation, horizontal flipping and re-use of the control lanes for the 35-week-old rats blot). In light of the concerns raised, the conclusions drawn in this article cannot be relied upon.
April 18, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29666943/the-gtn-patch-a-simple-and-effective-new-approach-to-cardioprotection
#11
Derek M Yellon, Zhenhe He, Rayomand Khambata, Amrita Ahluwalia, Sean M Davidson
There remains a significant un-met need to reduce the extent of myocardial injury caused by ischaemia and reperfusion injury in patients experiencing an ST-elevation MI. Although nitric oxide is central to many cardioprotective strategies currently undergoing investigation, cardioprotection from the delivery of nitrates/nitrites has been inconsistently observed. The route of administration appears to be a critical variable. The glyceryl trinitrate (GTN) patch is commonly used as a simple and practical means of delivering nitric oxide to patients with ischaemic heart disease, but whether acute cardioprotection can be achieved by application of a GTN patch has not been investigated before...
April 17, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29564567/t-bet-deficiency-attenuates-cardiac-remodelling-in-rats
#12
Zhen-Guo Ma, Jia Dai, Yu-Pei Yuan, Zhou-Yan Bian, Si-Chi Xu, Ya-Ge Jin, Xin Zhang, Qi-Zhu Tang
Previous studies have suggested the involvement of CD4 + T lymphocytes in cardiac remodelling. T-bet can direct Th1 lineage commitment. This study aimed to investigate the functional significance of T-bet in cardiac remodelling induced by pressure overload using T-bet global knockout rats. Increased T-bet levels were observed in rodent and human hypertrophied hearts. T-bet deficiency resulted in a less severe hypertrophic phenotype in rats. CD4 + T-lymphocyte reconstitution in T-bet-/- rats resulted in aggravated cardiac remodelling...
March 21, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29549541/role-of-the-angiotensin-converting-enzyme-in-the-g-csf-induced-mobilization-of-progenitor-cells
#13
Karin Kohlstedt, Caroline Trouvain, Timo Frömel, Thomas Mudersbach, Reinhard Henschler, Ingrid Fleming
In addition to being a peptidase, the angiotensin-converting enzyme (ACE) can be phosphorylated and involved in signal transduction. We evaluated the role of ACE in granulocyte-colony-stimulating factor (G-CSF)-induced hematopoietic progenitor cell (HPC) mobilization and detected a significant increase in mice-lacking ACE. Transplantation experiments revealed that the loss of ACE in the HPC microenvironment rather than in the HPCs increased mobilization. Indeed, although ACE was expressed by a small population of bone-marrow cells, it was more strongly expressed by endosteal bone...
March 17, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29546624/editorial-expression-of-concern-to-compensatory-role-of-the-nbcn1-sodium-bicarbonate-cotransporter-on-ca-2-induced-mitochondrial-swelling-in-hypertrophic-hearts
#14
EDITORIAL
Lorena A Vargas, Fernanda Carrizo Velasquez, Bernardo V Alvarez
No abstract text is available yet for this article.
March 15, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29524006/remote-ischemic-preconditioning-fails-to-reduce-infarct-size-in-the-zucker-fatty-rat-model-of-type-2-diabetes-role-of-defective-humoral-communication
#15
Joseph Wider, Vishnu V R Undyala, Peter Whittaker, James Woods, Xuequn Chen, Karin Przyklenk
Remote ischemic preconditioning (RIPC), the phenomenon whereby brief ischemic episodes in distant tissues or organs render the heart resistant to infarction, has been exhaustively demonstrated in preclinical models. Moreover, emerging evidence suggests that exosomes play a requisite role in conveying the cardioprotective signal from remote tissue to the myocardium. However, in cohorts displaying clinically common comorbidities-in particular, type-2 diabetes-the infarct-sparing effect of RIPC may be confounded for as-yet unknown reasons...
March 9, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29516255/25-years-of-remote-ischemic-conditioning-from-laboratory-curiosity-to-clinical-outcome
#16
EDITORIAL
Gerd Heusch
No abstract text is available yet for this article.
March 7, 2018: Basic Research in Cardiology
https://www.readbyqxmd.com/read/29516192/randomized-controlled-trial-of-remote-ischaemic-conditioning-in-st-elevation-myocardial-infarction-as-adjuvant-to-primary-angioplasty-ric-stemi
#17
António Gaspar, André P Lourenço, Miguel Álvares Pereira, Pedro Azevedo, Roberto Roncon-Albuquerque, Jorge Marques, Adelino F Leite-Moreira
To test whether remote ischaemic conditioning (RIC) as adjuvant to standard of care (SOC) would prevent progression towards heart failure (HF) after ST-elevation myocardial infarction (STEMI). Single-centre parallel 1:1 randomized trial (computerized block-randomization, concealed allocation) to assess superiority of RIC (3 cycles of intermittent 5 min lower limb ischaemia) over SOC in consecutive STEMI patients (NCT02313961, clinical trials.gov). From 258 patients randomized to RIC or SOC, 9 and 4% were excluded because of unconfirmed diagnosis and previously unrecognized exclusion criteria, respectively...
March 7, 2018: Basic Research in Cardiology
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
#18
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
#19
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
#20
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
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