Article
Cardiac & Cardiovascular Systems
Shan Ma, Ling Bai, Ping Liu, Gang She, Xiu-Ling Deng, An-Qi Song, Xiao-Jun Du, Qun Lu
Summary: Cardiac rupture and left ventricular thrombus after acute myocardial infarction may be linked in their pathogenesis, potentially triggered by a thrombo-inflammatory response following wall rupture or endocardial erosion.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2022)
Article
Cell Biology
Friedrich Reusswig, Amin Polzin, Meike Klier, Matthias Achim Dille, Aysel Ayhan, Marcel Benkhoff, Celina Lersch, Anika Prinz, Simone Gorressen, Jens Walter Fischer, Malte Kelm, Margitta Elvers
Summary: Platelets play a crucial role in thrombosis and inflammation after acute myocardial infarction (AMI). Acute thrombocytopenia can reduce infarct size and improve cardiac function, while chronic thrombocytopenia does not have a protective effect on heart function.
Review
Cell Biology
Yusra Zaidi, Eslie G. Aguilar, Miguel Troncoso, Daria Ilatovskaya, Kristine Y. DeLeon-Pennell
Summary: Myocardial infarction (MI) results in pathological changes in the left ventricle's extracellular matrix, which can cause cardiac stiffness and affect systolic and diastolic function. The signals released from necrotic tissue initiate an immune cascade and lead to inflammatory response and reparative fibrosis, with immune cells playing key roles in balancing pro-fibrotic and anti-fibrotic responses. This review explores how molecular signals between fibroblasts and immune cells regulate fibrosis post-MI, and discusses emerging pharmacological targets and therapies for inflammation and cardiac fibrosis associated with MI.
CELLULAR SIGNALLING
(2021)
Review
Cell Biology
Kyoko Komai, Nicholas K. Kawasaki, Jason K. Higa, Takashi Matsui
Summary: Ferroptosis is an iron-dependent form of regulated cell death characterized by dysfunction of the GPX4 antioxidant system. Inhibiting ferroptosis restores cardiac function and provides protection against I/R injury.
Article
Medicine, Research & Experimental
Bochra Tourki, Laurence M. Black, Vasundhara Kain, Ganesh Halade
Summary: The persistent increase in 12/15 lipoxygenase enzyme activity is associated with uncontrolled inflammation, which can lead to organ dysfunction. The use of the ML351 antagonist to inhibit lipoxygenases can suppress inflammation initiation but may also disrupt the acute immune response.
BIOMEDICINE & PHARMACOTHERAPY
(2021)
Review
Cardiac & Cardiovascular Systems
Daniele Ronco, Matteo Matteucci, Justine M. Ravaux, Silvia Marra, Federica Torchio, Claudio Corazzari, Giulio Massimi, Cesare Beghi, Jos Maessen, Roberto Lorusso
Summary: Ventricular septal rupture (VSR) is a rare complication of acute myocardial infarction, often leading to cardiogenic shock and high in-hospital mortality. Mechanical circulatory support (MCS) may enhance hemodynamic stabilization and delay VSR treatment, but the actual effects and interactions should be carefully assessed.
JACC-CARDIOVASCULAR INTERVENTIONS
(2021)
Review
Cardiac & Cardiovascular Systems
Joyce Lim, Allan Davies, Stephen Brienesse, Nishani S. Mabotuwana, Andrew Boyle
Summary: This systematic review investigates the association between leukocyte response and outcomes in patients with STEMI. The findings suggest that leukocyte count is associated with the occurrence of MACE within 30 days and 1 year. However, the high heterogeneity among studies limits the generalizability of these findings and further research is needed.
INTERNATIONAL JOURNAL OF CARDIOLOGY
(2023)
Article
Cardiac & Cardiovascular Systems
Jan Philipp Schuette, Mailin-Christin Manke, Katherina Hemmen, Patrick Muenzer, Barbara F. Schoerg, Gustavo Campos Ramos, Michaela Pogoda, Valerie Dicenta, Sabrina H. L. Hoffmann, Juergen Pinnecker, Ferdinand Kollotzek, Monika Zdanyte, Karin A. L. Mueller, Yogesh Singh, Andreas F. Mack, Bernd Pichler, Florian Lang, Bernhard Nieswandt, Meinrad Gawaz, Katrin G. Heinze, Nicolas Casadei, Oliver Borst
Summary: Platelet-derived miRNAs play a critical role in myocardial inflammation and structural remodeling in response to myocardial ischemia/reperfusion (I/R). In a mouse model with a Dicer gene deletion, disrupted miRNA processing machinery in platelets led to increased myocardial inflammation, impaired angiogenesis, accelerated cardiac fibrosis, and larger infarct size. These findings highlight the importance of platelet-derived miRNA in regulating cellular processes following myocardial I/R.
CIRCULATION RESEARCH
(2023)
Review
Cardiac & Cardiovascular Systems
Stefan Frantz, Moritz Jens Hundertmark, Jeanette Schulz-Menger, Frank Michael Bengel, Johann Bauersachs
Summary: Most patients survive acute myocardial infarction, but the prevalence of heart failure is increasing, leading to economic strain on healthcare systems. Pathological changes in the heart significantly impact patient outcomes. Risk factors like diabetes, chronic obstructive pulmonary disease, and female sex can distinctively shape the progression towards heart failure.
EUROPEAN HEART JOURNAL
(2022)
Article
Pharmacology & Pharmacy
Aoife B. Kilgallen, Frederieke van den Akker, Dries A. M. Feyen, Sandra Crnko, Christian J. B. Snijders Blok, Hendrik Gremmels, Bastiaan C. du Pre, Robin Reijers, Pieter A. Doevendans, Saskia C. A. de Jager, Joost P. G. Sluijter, Vasco Sampaio-Pinto, Linda W. van Laake
Summary: Circadian rhythms play a crucial role in the hyperacute immune response after a myocardial infarction (MI). The levels of immune cells and cardiac damage vary throughout the day, indicating the circadian influence on the immune response. These findings align with the clinical observation that patients who experience an MI early in the morning have worse outcomes.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Cardiac & Cardiovascular Systems
Elvira Forte, Bryant Perkins, Amalia Sintou, Harkaran S. Kalkat, Angelos Papanikolaou, Catherine Jenkins, Mashael Alsubaie, Rasheda A. Chowdhury, Theodore M. Duffy, Daniel A. Skelly, Jane Branca, Mohamed Bellahcene, Michael D. Schneider, Sian E. Harding, Milena B. Furtado, Fu Siong Ng, Muneer G. Hasham, Nadia Rosenthal, Susanne Sattler
Summary: After ischemic injury to the heart, cross-priming dendritic cells play a role in activating cytotoxic CD8(+) T cells by presenting self-antigens from necrotic cardiac cells. Research suggests that activation of cytotoxic CD8(+) T cells by cross-priming DC may exacerbate inflammatory damage of the myocardium and corresponding decline in cardiac function.
Article
Oncology
Adam Corken, Sanchita P. Ghosh, Ruofei Du, Marjan Boerma, Jerry Ware, Rupak Pathak
Summary: The study revealed that the lack of functional platelet GPIb alpha enhances radiation toxicity, leading to higher radiation lethality and more severe inflammatory response, as well as exacerbating intestinal damage. These findings suggest that GPIb alpha-mediated interactions play a crucial role in limiting radiation injury.
RADIOTHERAPY AND ONCOLOGY
(2022)
Article
Medicine, Research & Experimental
Xia Lu, Boshen Yang, Ruiqiang Qi, Qifei Xie, Taixi Li, Jie Yang, Tingting Tong, Kaifan Niu, Mingyu Li, Weijun Pan, Yongxin Zhang, Dongmei Shi, Suiji Li, Cuilian Dai, Chengxing Shen, Xiaoqing Wang, Yan Wang, Juan Song
Summary: WWP1 is upregulated in cardiomyocytes post-MI and under hypoxic conditions, and its overexpression promotes cardiomyocyte apoptosis and exacerbates cardiac dysfunction. Inhibiting WWP1 in cardiomyocytes protects against MI-induced cardiac ischemic injury.
Article
Biochemistry & Molecular Biology
Joseph Aliaga, Aldo Bonaventura, Eleonora Mezzaroma, Yogesh Dhakal, Adolfo Gabriele Mauro, Antonio Abbate, Stefano Toldo
Summary: The study suggests that using the NLRP3 inhibitor OLT1177(R) can protect cardiac function post myocardial infarction, including contractile reserve and diastolic function. This treatment may be beneficial in preventing heart failure development in patients with ischemic cardiomyopathy. The results demonstrate that OLT1177(R) can preserve beta-adrenergic responsiveness and prevent left ventricular diastolic dysfunction.
Review
Cardiac & Cardiovascular Systems
Danielle M. Coenen, Alexandra C. A. Heinzmann, Mieke F. A. Karel, Judith M. E. M. Cosemans, Rory R. Koenen
Summary: Atherosclerosis is a major contributor to various cardiovascular diseases, characterized by plaques and arterial wall thickening. Platelets play a crucial role in both the later stages of atherosclerosis, such as thrombotic occlusion, and in the earlier stages by exhibiting pro-inflammatory activities.
Article
Biochemistry & Molecular Biology
Taide Wang, Doris Tomas, Nirma D. Perera, Brittany Cuic, Sophia Luikinga, Aida Viden, Samantha K. Barton, Catriona A. McLean, Andre L. Samson, Adam Southon, Ashley I. Bush, James M. Murphy, Bradley J. Turner
Summary: Amyotrophic lateral sclerosis (ALS) is characterized by selective degeneration of motor neurons in the brain and spinal cord, with recent findings suggesting a role for ferroptosis, an iron-dependent form of regulated cell death, in mediating motor neuron death in ALS. Depletion of the antioxidant enzyme GPX4, a central repressor of ferroptosis, was observed in post-mortem spinal cords of ALS patients and in various ALS mouse models, linking GPX4 depletion and ferroptosis to impaired NRF2 signaling and dysregulation of glutathione synthesis and iron-binding proteins. Overexpression of human GPX4 in ALS mice delayed disease onset, improved locomotor function, and prolonged lifespan, demonstrating the potential for anti-ferroptotic therapeutic strategies for ALS treatment.
CELL DEATH AND DIFFERENTIATION
(2022)
Article
Biochemistry & Molecular Biology
Ashish Sethi, Christopher R. Horne, Cheree Fitzgibbon, Karyn Wilde, Katherine A. Davies, Sarah E. Garnish, Annette Jacobsen, Andre L. Samson, Joanne M. Hildebrand, Ahmad Wardak, Peter E. Czabotar, Emma J. Petrie, Paul R. Gooley, James M. Murphy
Summary: Necroptosis is a programmed cell death pathway that is often deregulated in inflammatory diseases. This study identifies the membrane binding epitope of mouse MLKL and reveals differences in structure and epitope between mouse and human MLKL. These findings highlight the versatility of the 4HB domain.
CELL DEATH AND DIFFERENTIATION
(2022)
Article
Cell Biology
Annette Jacobsen, Catia L. Pierotti, Kym N. Lowes, Amanda E. Au, Ying Zhang, Nima Etemadi, Cheree Fitzgibbon, Wilhelmus J. A. Kersten, Andre L. Samson, Mark F. van Delft, David C. S. Huang, Helene Jousset Sabroux, Guillaume Lessene, John Silke, James M. Murphy
Summary: The Lck inhibitor AMG-47a has been identified as an inhibitor of necroptosis, particularly effective in human cells. Additionally, RIPK1 is found to play a complete dependence in cell death caused by activated MLKL, with some involvement from RIPK3.
CELL DEATH & DISEASE
(2022)
Article
Biochemistry & Molecular Biology
Stefanie M. Bader, Simon P. Preston, Katie Saliba, Adam Lipszyc, Zoe L. Grant, Liana Mackiewicz, Andrew Baldi, Anne Hempel, Michelle P. Clark, Thanushi Peiris, William Clow, Jan Bjelic, Michael D. Stutz, Philip Arandjelovic, Jack Teale, Fashuo Du, Leigh Coultas, James M. Murphy, Cody C. Allison, Marc Pellegrini, Andre L. Samson
Summary: Caspase-8 mediates various responses including inflammation, cell proliferation, and cell death. Its function during embryogenesis is essential for maintaining systemic circulatory system, while in adulthood it is crucial for preserving gut vascular integrity. Lack of endothelial Caspase-8 leads to fatal hemorrhagic lesions in the small intestine, resulting from aberrant microbial sensing and tumor necrosis factor receptor signaling.
CELL DEATH AND DIFFERENTIATION
(2023)
Review
Cell Biology
Christopher R. Horne, Andre L. Samson, James M. Murphy
Summary: In the past decade, the importance of the necroptosis programmed cell death pathway in the pathophysiology of various diseases has been confirmed. The receptor interacting protein kinase (RIPK)1 and RIPK3, and the pseudokinase executioner protein, mixed lineage kinase domain-like (MLKL), have emerged as core components of the pathway. These proteins also serve as integrators of signals and add complexity to pathway regulation. This article describes the emerging concept of the protein network that tunes necroptotic signal transduction and how these events have diverged across species, possibly due to selective pressures from pathogens on the RIPK3-MLKL protein pair.
TRENDS IN CELL BIOLOGY
(2023)
Letter
Hematology
Marc L. Ellis, Imala Alwis, Rhyll Smythe, Yuping Yuan, Shaun P. Jackson
Article
Biochemistry & Molecular Biology
Emma C. Tovey C. Crutchfield, Sarah E. Garnish, Jessica Day, Holly Anderton, Shene Chiou, Anne Hempel, Cathrine Hall, Komal M. Patel, Pradnya Gangatirkar, Katherine R. Martin, Connie S. N. Li Wai Suen, Alexandra L. Garnham, Andrew J. Kueh, Ian P. Wicks, John Silke, Ueli Nachbur, Andre L. Samson, James M. Murphy, Joanne M. Hildebrand
Summary: MLKL and RIPK3 are core signaling proteins of the necroptosis pathway, which is involved in human disease. Necroptosis has been implicated in disease progression in multiple physiological systems and recent studies suggest its role in aging. In this study, we analyzed age-related histopathological and immunological phenotypes in Mlkl(-/-) and Ripk3(-/-) mice. We found that female Mlkl(-/-) mice showed delayed immune system aging and reduced age-related chronic sterile inflammation compared to wild-type mice. These findings suggest a possible application of anti-necroptotic therapy in age-related inflammation.
CELL DEATH AND DIFFERENTIATION
(2023)
Editorial Material
Surgery
Leonard L. Shan
EUROPEAN JOURNAL OF VASCULAR AND ENDOVASCULAR SURGERY
(2023)
Meeting Abstract
Surgery
L. L. Shan, L. S. Yang, M. Tew, M. J. Westcott, T. D. Spelman, P. F. Choong, A. H. Davies
JOURNAL OF VASCULAR SURGERY
(2023)
Article
Surgery
Leonard L. Shan, Stacey Telianidis, Mark J. Westcott, Deborah Debono, Alun H. Davies, Peter F. Choong
Summary: This study conducted qualitative research and engaged patients to gain insights into the quality of life perspectives of CLTI patients. The results provide important understanding of what quality of life truly means to CLTI patients and what factors are important to their quality of life.
ANZ JOURNAL OF SURGERY
(2023)
