Review
Cell Biology
Akihiko Kubota, Nikolaos G. Frangogiannis
Summary: Following myocardial infarction, macrophages play important roles in both injurious and reparative responses. They regulate the inflammatory response through phagocytosis and secretion of mediators, and contribute to the repair of the infarcted heart. However, the relationship between transcriptomic profiles and functional properties of macrophages in infarcted hearts is still unclear.
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
(2022)
Article
Genetics & Heredity
Jianwei Li, Hua Qu, Yong Wang
Summary: Acute myocardial infarction (AMI) is a major cause of death worldwide, with inflammation being a key contributor to its pathophysiology. Amplified in breast 1 (Aib1) is a transcriptional coactivator protein with anti-inflammatory effects. However, the role of Aib1 in AMI has not been described yet. In this study, Aib1 deficiency was found to exacerbate infarction, cardiac dysfunction, and inflammation in AMI mice, indicating the importance of Aib1 in regulating inflammation in AMI.
JOURNAL OF MOLECULAR MEDICINE-JMM
(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.
Article
Biochemistry & Molecular Biology
Jishou Zhang, Yao Xu, Cheng Wei, Zheng Yin, Wei Pan, Mengmeng Zhao, Wen Ding, Shuwan Xu, Jianfang Liu, Junping Yu, Jing Ye, Di Ye, Juan-Juan Qin, Jun Wan, Menglong Wang
Summary: This study found that Neo1 deficiency aggravates inflammation and left ventricular remodeling after myocardial infarction by modulating macrophage phenotypes and functions via the JAK1-STAT1 signaling pathway. These findings offer new perspectives for therapeutic targets in myocardial infarction treatment.
CELLULAR AND MOLECULAR LIFE SCIENCES
(2023)
Review
Medicine, General & Internal
Mohammad Alkhalil, Giovanni Luigi De Maria, Naveed Akbar, Neil Ruparelia, Robin P. Choudhury
Summary: The past decade has witnessed significant advancements in the understanding of acute myocardial infarction (AMI) and the systemic inflammatory response it triggers. Despite this, clinical decision making still heavily relies on traditional assessments based on chest pain onset, electrocardiogram findings, and troponin measurements. However, emerging techniques such as myocardial imaging, physiological measures, and blood biomarkers offer opportunities for improved diagnostic stratification and rational therapeutic interventions in AMI. Integrating these tools will be key in developing a comprehensive understanding of patient-level processes in myocardial injury and repair.
JOURNAL OF CLINICAL MEDICINE
(2023)
Review
Cardiac & Cardiovascular Systems
Xuekun Wu, Marc R. Reboll, Mortimer Korf-Klingebiel, Kai C. Wollert
Summary: The translation describes how acute myocardial infarction causes damage to the coronary microcirculation, leading to vascular disintegration and capillary rarefication in the infarct region. Tissue repair after MI involves robust angiogenic response and interactions among various cell types through secreted proteins and receptors. Macrophages and fibroblasts have emerged as major drivers of the angiogenic response after MI, while understanding the mechanism of infarct angiogenesis creates therapeutic opportunities.
CARDIOVASCULAR RESEARCH
(2021)
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)
Article
Medicine, Research & Experimental
Rudolf A. Werner, Annika Hess, Tobias Koenig, Johanna Diekmann, Thorsten Derlin, Anette Melk, James T. Thackeray, Johann Bauersachs, Frank M. Bengel
Summary: The study revealed transient myocardial CXCR4 upregulation early after MI. The PET signals in the heart and kidneys were directly correlated, suggesting inflammatory crosstalk between the organs. In patients, renal CXCR4 signal was also associated with infarct and remote myocardium signals.
Review
Cardiac & Cardiovascular Systems
Michael A. Matter, Francesco Paneni, Peter Libby, Stefan Frantz, Barbara E. Stahli, Christian Templin, Alessandro Mengozzi, Yu-Jen Wang, Thomas M. Kundig, Lorenz Raber, Frank Ruschitzka, Christian M. Matter
Summary: The role of pro-inflammatory pathways in coronary artery disease has been confirmed by convergent experimental and clinical evidence. The interest in treating inflammation in patients suffering from acute myocardial infarction (AMI) is expanding from chronic aspects to acute setting. Large outcome trials have shown the benefits of anti-inflammatory therapies on cardiovascular outcomes by targeting residual inflammatory risk (RIR) in the late phase after AMI. However, there are potential risks associated with anti-inflammatory therapy after AMI, particularly related to impaired host defence. Smaller-scale trials have demonstrated varied degrees of success when targeting excessive inflammation in the early phase after AMI, especially through the interleukin-1 and -6 pathways. Lessons learnt from past research may inform an optimized approach to target post-AMI inflammation, tailored to spare repair and defence while treating residual inflammation and capturing excessive inflammation in the acute phase. Rigorous clinical trials are needed to test this approach.
EUROPEAN HEART JOURNAL
(2023)
Article
Pharmacology & Pharmacy
Huiqin Hao, Tao Yuan, Zexin Li, Chenglin Zhang, Jie Liu, Guang Liang, Li Feng, Yong Pan
Summary: This study found that the curcumin analogue C66 has protective effects against acute myocardial infarction by inhibiting tissue inflammation and cardiomyocyte apoptosis, improving cardiac function, and reducing infarct size. C66 also alleviates cardiac hypertrophy and fibrosis. The mechanism involves the inhibition of JNK phosphorylation by C66.
EUROPEAN JOURNAL OF PHARMACOLOGY
(2023)
Article
Cardiac & Cardiovascular Systems
Wolfgang Ries, Jan Torzewski, Franz Heigl, Christian Pfluecke, Sebastian Kelle, Harald Darius, Hueseyin Ince, Steffen Mitzner, Peter Nordbeck, Christian Butter, Horst Skarabis, Ahmed Sheriff, Christoph D. Garlichs
Summary: This study aimed to investigate the relationship between CRP levels, myocardial infarct size and function, and the safety and efficacy of CRP apheresis in STEMI patients. The results showed significant differences in the correlation between CRP concentration and infarct size, as well as LV function, between the CRP apheresis group and the control group. CRP apheresis effectively reduced CRP levels without relevant side effects and has the potential to interfere with deleterious aspects of STEMI.
FRONTIERS IN CARDIOVASCULAR MEDICINE
(2021)
Article
Clinical Neurology
Thomas Bochaton, Simon Leboube, Alexandre Paccalet, Claire Crola Da Silva, Marielle Buisson, Nathan Mewton, Camille Amaz, Yvonne Varillon, Eric Bonnefoy-Cudraz, Gilles Rioufol, Tae-Hee Cho, Michel Ovize, Gabriel Bidaux, Norbert Nighoghossian, Laura Mechtouff
Summary: This study compared the profile of circulating inflammatory markers between young and older patients with STEMI or AIS. The results showed that older patients had higher levels of IL-6 and sTNF-RI within the first 48 hours, accompanied by a lower lymphocyte count and a higher neutrophil-lymphocyte ratio.
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
Medicine, Research & Experimental
Marta Paz-Garcia, Adrian Povo-Retana, Rafael I. Jaen, Patricia Prieto, Diego A. Peraza, Carlos Zaragoza, Macarena Hernandez-Jimenez, David Pineiro, Javier Regadera, Maria L. Garcia-Bermejo, E. Macarena Rodriguez-Serrano, Sergio Sanchez-Garcia, Maria A. Moro, Ignacio Lizasoain, Carmen Delgado, Carmen Valenzuela, Lisardo Bosca
Summary: Experimental evidence suggests that controlling the inflammatory response is crucial in reducing cardiac injury after myocardial infarction. An aptamer called 4FT has been investigated for its selective antagonistic effects on human TLR4 in macrophages and a rat model of cardiac ischemia/reperfusion. Treatment with 4FT significantly inhibits TLR4 signaling and improves cardiac injury and markers in the rat model. The expression of inflammatory genes is reduced, while anti-inflammatory genes and pro-resolution molecules are enhanced after 4FT administration, indicating its potential as a therapeutic strategy for preventing cardiac dysfunction after infarction.
BIOMEDICINE & PHARMACOTHERAPY
(2023)
Article
Medicine, General & Internal
Lei Li, Jingjing Wang, Wei Huang, Jun Zhang
Summary: Morroniside effectively promotes angiogenesis in rats with acute myocardial infarction by regulating pro-angiogenic growth factors and related proteins in the downstream ERK1/2 signaling pathway of VEGF.
ACTA MEDICA MEDITERRANEA
(2021)
