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https://www.readbyqxmd.com/read/28212151/antibody-mediated-rejection-in-the-cardiac-allograft-diagnosis-treatment-and-future-considerations
#1
M Elizabeth H Hammond, Abdallah G Kfoury
PURPOSE OF REVIEW: This review summarizes the latest publications dealing with antibody-mediated rejection (AMR) and defines areas of controversy and future steps that may improve the outcome for patients with this virulent form of rejection. RECENT FINDINGS: Recent progress includes publication of standardized pathologic criteria for acute AMR by the International Society for Heart and Lung Transplantation (ISHLT) and guidelines for treatment of acute AMR by the American Heart Association, endorsed by ISHLT as well...
February 15, 2017: Current Opinion in Cardiology
https://www.readbyqxmd.com/read/28202417/triptolide-attenuates-pressure-overload-induced-myocardial-remodeling-in-mice-via-the-inhibition-of-nlrp3-inflammasome-expression
#2
Rujun Li, Kuiying Lu, Yao Wang, Mingxing Chen, Fengyu Zhang, Hui Sheng, Deshan Yao, Kaizheng Gong, Zhengang Zhang
Triptolide is the predominant active component of the Chinese herb Tripterygium wilfordii Hook F (TwHF) that has been widely used to treat several chronic inflammatory diseases due to its immunosuppressive, anti-inflammatory, and anti-proliferative properties. In the present study, we elucidated the cardioprotective effects of triptolide against cardiac dysfunction and myocardial remodeling in chronic pressure-overloaded hearts. Furthermore, the potential mechanisms of triptolide were investigated. For this purpose, C57/BL6 mice were anesthetized and subjected to transverse aortic constriction (TAC) or sham operation...
February 12, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28194569/the-role-of-inflammation-in-cardiovascular-outcome
#3
REVIEW
Fabrizio Montecucco, Luca Liberale, Aldo Bonaventura, Alessandra Vecchiè, Franco Dallegri, Federico Carbone
PURPOSE OF REVIEW: The aim of this review is to update the pathophysiological role of innate immune response in the cardiovascular (CV) disease outcomes, particularly focusing on coronary atherosclerosis and heart failure. RECENT FINDINGS: Inflammatory processes comprised with the innate immunity reaction are believed to actively trigger CV disease development and final clinical events. For instance, by releasing proteases and neutrophil extracellular traps, neutrophil recruitment and activation might strongly influence atherosclerotic plaque stability...
March 2017: Current Atherosclerosis Reports
https://www.readbyqxmd.com/read/28193608/dectin-2-deficiency-modulates-th1-differentiation-and-improves-wound-healing-after-myocardial-infarction
#4
Xiaoxiang Yan, Hang Zhang, Qin Fan, Jian Hu, Rong Tao, Qiujing Chen, Yoichiro Iwakura, Weifeng Shen, Lin Lu, Qi Zhang, Ruiyan Zhang
Rationale: Macrophages are involved in wound healing after myocardial infarction (MI). The role of Dectin-2, a pattern recognition receptor mainly expressed on myeloid cells, in the infarct healing remains unknown. Objective: To determine whether Dectin-2 signaling is involved in the healing process and cardiac remodeling after MI, and to elucidate the underlying molecular mechanisms. Methods and Results: In a mouse model of permanent coronary ligation, Dectin-2, mainly expressed in macrophages, was shown to be increased in the early phase after MI...
February 13, 2017: Circulation Research
https://www.readbyqxmd.com/read/28176833/transmissible-endoplasmic-reticulum-stress-from-myocardiocytes-to-macrophages-is-pivotal-for-the-pathogenesis-of-cvb3-induced-viral-myocarditis
#5
Hui Zhang, Yan Yue, Tianle Sun, Xuejie Wu, Sidong Xiong
Infiltrating macrophages have been proven as a pivotal pathological inflammatory cell subset in coxsackievirus B3 (CVB3) induced viral myocarditis. However, the mechanisms underlying the initiation and promotion of macrophage pro-inflammatory responses are still blur. We previously reported that cardiac ER stress contributed to CVB3-induced myocarditis by augmenting inflammation. In this study, we focused on the influence of ER stress on the macrophage inflammatory responses in the viral myocarditis. We found that ER stress was robustly induced in the cardiac infiltrating macrophages from CVB3-infected mice, and robustly facilitated the production of pro-inflammatory cytokines (IL-6, IL-12, MCP-1 and IP-10)...
February 8, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28174192/infarcted-myocardium-primed-dendritic-cells-improve-remodeling-and-cardiac-function-after-myocardial-infarction-by-modulating-the-treg-and-macrophage-polarization
#6
Eun Ho Choo, Jun-Ho Lee, Eun-Hye Park, Hyo Eun Park, Nam-Chul Jung, Tae-Hoon Kim, Yoon-Seok Koh, Eunmin Kim, Ki-Bae Seung, Cheongsoo Park, Kwan-Soo Hong, Kwonyoon Kang, Jie-Young Song, Han Geuk Seo, Dae-Seog Lim, Kiyuk Chang
BACKGROUND: -Inflammatory responses play a critical role in left ventricular (LV) remodeling after a myocardial infarction (MI). Tolerogenic dendritic cells (tDCs) can modulate immune responses inducing regulatory T cells (Tregs) in a number of inflammatory diseases. METHODS: -We generated tDCs by treating bone marrow-derived dendritic cells with TNF-α and cardiac lysate from MI mice. We injected MI mice, which were induced by a ligation of the left anterior descending coronary artery in C57BL/6 mice, twice with tDCs within 24 hours and at 7 days after the ligation...
February 7, 2017: Circulation
https://www.readbyqxmd.com/read/28173864/macrophage-activation-and-polarization-in-post-infarction-cardiac-remodeling
#7
REVIEW
Aleksandra Gombozhapova, Yuliya Rogovskaya, Vladimir Shurupov, Mariya Rebenkova, Julia Kzhyshkowska, Sergey V Popov, Rostislav S Karpov, Vyacheslav Ryabov
Adverse cardiac remodeling leads to impaired ventricular function and heart failure, remaining a major cause of mortality and morbidity in patients with acute myocardial infarction. It have been shown that, even if all the recommended therapies for ST-segment elevation myocardial infarction are performed, one third of patients undergoes progressive cardiac remodeling that represents morphological basis for following heart failure. The need to extend our knowledge about factors leading to different clinical scenarios of myocardial infarction and following complications has resulted in a research of immuno-inflammatory pathways and molecular activities as the basis for post-infarction remodeling...
February 7, 2017: Journal of Biomedical Science
https://www.readbyqxmd.com/read/28152512/klotho-suppresses-the-inflammatory-responses-and-ameliorates-cardiac-dysfunction-in-aging-endotoxemic-mice
#8
Haipeng Hui, Yufeng Zhai, Lihua Ao, Joseph C Cleveland, Hongbin Liu, David A Fullerton, Xianzhong Meng
BACKGROUND: Aging augments endotoxemic cardiac dysfunction, but the mechanism remains unclear. Anti-aging protein Klotho has been found to modulate tissue inflammatory responses. We tested the hypothesis that a reduced Klotho level in aging heart plays a role in the augmented endotoxemic cardiac dysfunction. MATERIALS AND METHODS: Endotoxin (0.5 mg/kg, iv) was injected to adults (4-6 months) and aging (18-20 months) C57BL/6 mice. Recombinant Klotho (10 μg/kg, iv) was administered to a group of aging mice after endotoxin injection...
February 1, 2017: Oncotarget
https://www.readbyqxmd.com/read/28141779/direct-targeting-of-macrophages-with-methylglyoxal-bis-guanylhydrazone-decreases-siv-associated-cardiovascular-inflammation-and-pathology
#9
Joshua A Walker, Andrew D Miller, Tricia H Burdo, Michael S McGrath, Kenneth C Williams
BACKGROUND: Despite effective combination antiretroviral therapy (cART) HIV infected individuals develop co-morbidities including cardiovascular disease (CVD), where activated macrophages play a key role. To date, few therapies target activated monocytes and macrophages. METHODS: We evaluated a novel oral form of the polyamine biosynthesis inhibitor methylglyoxal-bisguanylhydrazone (MGBG) on cardiovascular inflammation, carotid artery intima-media thickness (cIMT), and fibrosis in a SIV infection model of AIDS...
January 30, 2017: Journal of Acquired Immune Deficiency Syndromes: JAIDS
https://www.readbyqxmd.com/read/28132924/dapagliflozin-a-selective-sglt2-inhibitor-attenuated-cardiac-fibrosis-by-regulating-the-macrophage-polarization-via-stat3-signaling-in-infarcted-rat-hearts
#10
Tsung-Ming Lee, Nen-Chung Chang, Shinn-Zong Lin
During myocardial infarction, infiltrated macrophages have pivotal roles in cardiac remodeling and delayed M1 toward M2 macrophage phenotype transition is considered one of the major factors for adverse ventricular remodeling. We investigated whether dapagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, attenuates cardiac fibrosis via regulating macrophage phenotype by a reactive oxygen and nitrogen species (RONS)/STAT3-dependent pathway in postinfarcted rats. Normoglycemic male Wistar rats were subjected to coronary ligation and then randomized to either saline, dapagliflozin (a specific SGLT2 inhibitor), phlorizin (a nonspecific SGLT1/2 inhibitor), dapagliflozin + S3I-201 (a STAT3 inhibitor), or phlorizin + S3I-201 for 4 weeks...
January 26, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28131704/notch3-deficiency-impairs-coronary-microvascular-maturation-and-reduces-cardiac-recovery-after-myocardial-ischemia
#11
Yong-Kang Tao, Heng Zeng, Guo-Qiang Zhang, Sean T Chen, Xue-Jiao Xie, Xiaochen He, Shuo Wang, Hongyan Wen, Jian-Xiong Chen
RATIONALE: Vascular maturation plays an important role in wound repair post-myocardial infarction (MI). The Notch3 is critical for pericyte recruitment and vascular maturation during embryonic development. OBJECTIVE: This study is to test whether Notch3 deficiency impairs vascular maturation and blunts cardiac functional recovery post-MI. APPROACH AND RESULTS: Wild type (WT) and Notch3 knockout (Notch3KO) mice were subjected to MI by the ligation of left anterior descending coronary artery (LAD)...
January 24, 2017: International Journal of Cardiology
https://www.readbyqxmd.com/read/28129114/macrophage-derived-mir-155-containing-exosomes-suppress-fibroblast-proliferation-and-promote-fibroblast-inflammation-during-cardiac-injury
#12
Chunxiao Wang, Congcong Zhang, Luxin Liu, Xi A, Boya Chen, Yulin Li, Jie Du
Inflammation plays an important role in cardiac injuries. Here, we examined the role of miRNA in regulating inflammation and cardiac injury during myocardial infarction. We showed that mir-155 expression was increased in the mouse heart after myocardial infarction. Upregulated mir-155 was primarily presented in macrophages and cardiac fibroblasts of injured hearts, while pri-mir-155 was only expressed in macrophages. mir-155 was also presented in exosomes derived from macrophages, and it can be transferred into cardiac fibroblasts by macrophage-derived exosomes...
January 4, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/28125666/mononuclear-phagocytes-are-dispensable-for-cardiac-remodeling-in-established-pressure-overload-heart-failure
#13
Bindiya Patel, Mohamed Ameen Ismahil, Tariq Hamid, Shyam S Bansal, Sumanth D Prabhu
BACKGROUND: Although cardiac and splenic mononuclear phagocytes (MPs), i.e., monocytes, macrophages and dendritic cells (DCs), are key contributors to cardiac remodeling after myocardial infarction, their role in pressure-overload remodeling is unclear. We tested the hypothesis that these immune cells are required for the progression of remodeling in pressure-overload heart failure (HF), and that MP depletion would ameliorate remodeling. METHODS AND RESULTS: C57BL/6 mice were subjected to transverse aortic constriction (TAC) or sham operation, and assessed for alterations in MPs...
2017: PloS One
https://www.readbyqxmd.com/read/28112757/reversal-of-maladaptive-fibrosis-and-compromised-ventricular-function-in-the-pressure-overloaded-heart-by-a-caveolin-1-surrogate-peptide
#14
Dorea Pleasant-Jenkins, Charles Reese, Panneerselvem Chinnakkannu, Harinath Kasiganesan, Elena Tourkina, Stanley Hoffman, Dhandapani Kuppuswamy
Chronic ventricular pressure overload (PO) results in congestive heart failure (CHF) in which myocardial fibrosis develops in concert with ventricular dysfunction. Caveolin-1 is important in fibrosis in various tissues due to its decreased expression in fibroblasts and monocytes. The profibrotic effects of low caveolin-1 can be blocked with the caveolin-1 scaffolding domain peptide (CSD, a caveolin-1 surrogate) using both mouse models and human cells. We have studied the beneficial effects of CSD on mice in which PO was induced by trans-aortic constriction (TAC)...
January 23, 2017: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/28111317/transplantation-of-adipose-derived-stem-cells-combined-with-neuregulin-microparticles-promotes-efficient-cardiac-repair-in-a-rat-myocardial-infarction-model
#15
Paula Díaz-Herráez, Laura Saludas, Simón Pascual-Gil, Teresa Simón-Yarza, Gloria Abizanda, Felipe Prósper, Elisa Garbayo, María José Blanco-Prieto
Tissue engineering is a promising strategy to promote heart regeneration after a myocardial infarction (MI). In this study, we investigated the reparative potential of a system that combines adipose-derived stem cells (ADSCs) with microparticles (MPs) loaded with neuregulin (NRG), named ADSC-NRG-MPs, on a rat MI model. First, cells were attached to the surface of MPs encapsulating NRG and coated with a 1:1 mixture of collagen and poly-d-lysine. One week after in vivo administration, the system favored the shift of macrophage expression from a pro-inflammatory to a regenerative phenotype...
January 19, 2017: Journal of Controlled Release: Official Journal of the Controlled Release Society
https://www.readbyqxmd.com/read/28101763/mir-126-affects-brain-heart-interaction-after-cerebral-ischemic-stroke
#16
Jieli Chen, Chengcheng Cui, Xiaoping Yang, Jiang Xu, Poornima Venkat, Alex Zacharek, Peng Yu, Michael Chopp
Cardiovascular diseases are approximately three times higher in patients with neurological deficits than in patients without neurological deficits. MicroRNA-126 (MiR-126) facilitates vascular remodeling and decreases fibrosis and is emerging as an important factor in the pathogenesis of cardiovascular diseases and cerebral stroke. In this study, we tested the hypothesis that decreased miR-126 after ischemic stroke may play an important role in regulating cardiac function. Wild-type (WT), specific conditional-knockout endothelial cell miR-126 (miR-126(EC-/-)), and miR-126 knockout control (miR-126(fl/fl)) mice were subjected to distal middle cerebral artery occlusion (dMCAo) (n = 10/group)...
January 19, 2017: Translational Stroke Research
https://www.readbyqxmd.com/read/28091604/polyglucose-nanoparticles-with-renal-elimination-and-macrophage-avidity-facilitate-pet-imaging-in-ischaemic-heart-disease
#17
Edmund J Keliher, Yu-Xiang Ye, Gregory R Wojtkiewicz, Aaron D Aguirre, Benoit Tricot, Max L Senders, Hannah Groenen, Francois Fay, Carlos Perez-Medina, Claudia Calcagno, Giuseppe Carlucci, Thomas Reiner, Yuan Sun, Gabriel Courties, Yoshiko Iwamoto, Hye-Yeong Kim, Cuihua Wang, John W Chen, Filip K Swirski, Hsiao-Ying Wey, Jacob Hooker, Zahi A Fayad, Willem J M Mulder, Ralph Weissleder, Matthias Nahrendorf
Tissue macrophage numbers vary during health versus disease. Abundant inflammatory macrophages destruct tissues, leading to atherosclerosis, myocardial infarction and heart failure. Emerging therapeutic options create interest in monitoring macrophages in patients. Here we describe positron emission tomography (PET) imaging with (18)F-Macroflor, a modified polyglucose nanoparticle with high avidity for macrophages. Due to its small size, Macroflor is excreted renally, a prerequisite for imaging with the isotope flourine-18...
January 16, 2017: Nature Communications
https://www.readbyqxmd.com/read/28090291/macrophage-migration-inhibitory-factor-as-a-novel-biomarker-of-portopulmonary-hypertension
#18
Hilary M DuBrock, Josanna M Rodriguez-Lopez, Barbara L LeVarge, Michael P Curry, Paul A VanderLaan, Zsuzsanna K Zsengeller, Elizabeth Pernicone, Ioana R Preston, Paul B Yu, Ivana Nikolic, Dihua Xu, Ravi I Thadhani, Richard N Channick, S Ananth Karumanchi
Portopulmonary hypertension (POPH) is a poorly understood complication of liver disease associated with significant morbidity and mortality. We sought to identify novel biomarkers of POPH disease presence and severity. We performed a prospective, multicenter, case-control study involving patients with liver disease undergoing right heart catheterization. POPH cases were defined as a mean pulmonary arterial pressure (mPAP) ≥25 mmHg and pulmonary vascular resistance (PVR) >240 dynes˙s˙cm(-5). Plasma samples were collected from the systemic and pulmonary circulation, and antibody microarray was used to identify biomarkers...
December 2016: Pulmonary Circulation
https://www.readbyqxmd.com/read/28087471/il-6-promotes-m2-macrophage-polarization-by-modulating-purinergic-signaling-and-regulates-the-lethal-release-of-nitric-oxide-during-trypanosoma-cruzi-infection
#19
Liliana M Sanmarco, Nicolás E Ponce, Laura M Visconti, Natalia Eberhardt, Martin G Theumer, Ángel R Minguez, Maria P Aoki
The production of nitric oxide (NO) is a key defense mechanism against intracellular pathogens but it must be tightly controlled in order to avoid excessive detrimental oxidative stress. In this study we described a novel mechanism through which interleukin (IL)-6 mediates the regulation of NO release induced in response to Trypanosoma cruzi infection. Using a murine model of Chagas disease, we found that, in contrast to C57BL/6 wild type (WT) mice, IL-6-deficient (IL6KO) mice exhibited a dramatic increase in plasma NO levels concomitant with a significantly higher amount of circulating IL-1β and inflammatory monocytes...
January 11, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28086885/harnessing-the-early-post-injury-inflammatory-responses-for-cardiac-regeneration
#20
REVIEW
Bill Cheng, H C Chen, I W Chou, Tony W H Tang, Patrick C H Hsieh
Cardiac inflammation is considered by many as the main driving force in prolonging the pathological condition in the heart after myocardial infarction. Immediately after cardiac ischemic injury, neutrophils are the first innate immune cells recruited to the ischemic myocardium within the first 24 h. Once they have infiltrated the injured myocardium, neutrophils would then secret proteases that promote cardiac remodeling and chemokines that enhance the recruitment of monocytes from the spleen, in which the recruitment peaks at 72 h after myocardial infarction...
January 13, 2017: Journal of Biomedical Science
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