Review
Biochemistry & Molecular Biology
Jamie Francisco, Dominic P. Del Re
Summary: Acute myocardial infarction (MI) is a condition that causes cardiac damage and cell loss. Restoring coronary flow is the standard treatment for MI, but reperfusion triggers inflammation and worsens heart injury. The immune response plays a crucial role in the pathogenesis and resolution of ischemia/reperfusion (I/R) injury, but our understanding is still incomplete.
Article
Biochemistry & Molecular Biology
Daniel I. Bromage, Silvia C. Trevelin, Josef Huntington, Victoria X. Yang, Ananya Muthukumar, Sarah J. Mackie, Greta Sawyer, Xiaohong Zhang, Celio X. C. Santos, Niloufar Safinia, Ioannis Smyrnias, Mauro Giacca, Aleksandar Ivetic, Ajay M. Shah
Summary: Dysregulated inflammation is implicated in ventricular remodeling and heart failure after myocardial infarction (MI). Transcription factor Nrf2 is a promising target as it inhibits pro-inflammatory cytokines and has anti-inflammatory effects.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(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)
Review
Immunology
Jiarong Gu, Hao Xu, Yandong Chen, Na Li, Xin Hou
Summary: This article reviews the biosynthesis and functions of miR-223 in innate immunity, highlighting its key role in inflammatory diseases and cancers. Furthermore, it discusses the potential role of miR-223 in liver physiopathology and therapeutic prospects.
FRONTIERS IN IMMUNOLOGY
(2022)
Article
Biochemistry & Molecular Biology
Tao Wang, Mengyuan Yu, Hangzhuo Li, Shuguang Qin, Wujing Ren, Yixuan Ma, Wenyan Bo, Yue Xi, Mengxin Cai, Zhenjun Tian
Summary: Myocardial infarction (MI) causes peripheral organ injury, known as cardiac hepatopathy. Aerobic exercise (AE) effectively improves liver injury, by activating the FNDC5/irisin-PI3K/Akt signaling pathway, promoting M2 macrophage polarization and inhibiting liver inflammation. Irisin, derived from FNDC5 cleavage, plays a key role in the beneficial effects of AE.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Biochemistry & Molecular Biology
Yanhai Wang
Summary: The incidence of myocardial infarction (MI) is increasing worldwide. Incorporating circulating biomarkers with other diagnostic techniques is crucial for evaluating, predicting, and assessing therapeutic efficacy of MI patients. Biomarker evaluation has been used in MI diagnosis for over 50 years, and further research can be done to explore newer biomarkers that initiate earlier than current ones. Understanding the complex pathophysiology of MI has led to a search for innovative biomarkers that can overcome the limitations of current ones and personalize treatment for high-risk individuals. This review focuses on biomarkers that offer diagnostic and prognostic information, as well as theoretical advancements in cardiovascular immunotherapy.
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
(2023)
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)
Review
Biochemistry & Molecular Biology
Wenjie Zuo, Renhua Sun, Zhenjun Ji, Genshan Ma
Summary: Macrophages play a crucial role in the inflammatory repair process following myocardial infarction. The traditional classification of macrophages as either pro-inflammatory or pro-reparative falls short of precision medicine standards. Advances in single-cell sequencing technology have opened new avenues for studying macrophage heterogeneity and plasticity.
CELLULAR & MOLECULAR BIOLOGY LETTERS
(2023)
Article
Radiology, Nuclear Medicine & Medical Imaging
Mark G. MacAskill, Agne Stadulyte, Lewis Williams, Timaeus E. F. Morgan, Nikki L. Sloan, Carlos J. Alcaide-Corral, Tashfeen Walton, Catriona Wimberley, Chris-Anne Mckenzie, Nick Spath, William Mungall, Ralph BouHaidar, Marc R. Dweck, Gillian A. Gray, David E. Newby, Christophe Lucatelli, Andrew Sutherland, Sally L. Pimlott, Adriana A. S. Tavares
Summary: F-18-LW223 is not susceptible to the rs6971 genetic polymorphism in vitro assays and shows favorable in vivo characteristics in detecting macrophage-driven inflammation after myocardial infarction. The radiotracer displayed specific uptake consistent with TSPO expression, slow metabolism in blood, high plasma free fraction, and suitable dosimetry profile in rodents. Additionally, F-18-LW223 binding potential was significantly higher in the myocardial infarction cohort compared to naive animals, indicating its potential clinical utility in accurately mapping inflammation.
JOURNAL OF NUCLEAR MEDICINE
(2021)
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)
Article
Biochemistry & Molecular Biology
Jun Li, Ruoshui Li, Izabela Tuleta, Silvia C. Hernandez, Claudio Humeres, Anis Hanna, Bijun Chen, Nikolaos G. Frangogiannis
Summary: The role of macrophage Smad7 in regulating inflammation and repair after myocardial infarction is limited. The anti-inflammatory effects of TGF-beta in macrophages are not restrained by endogenous Smad7 induction.
Article
Medicine, General & Internal
Bektas Murat, Selda Murat, Mehmet Ozgeyik, Muzaffer Bilgin
Summary: This study aimed to evaluate the association of Pan-Immune-Inflammation Value (PIV) with mortality in STEMI patients. The results showed that PIV is a better predictor of mortality in STEMI patients.
EUROPEAN JOURNAL OF CLINICAL INVESTIGATION
(2023)
Review
Cell Biology
Andreas Margraf, Mauro Perretti
Summary: This article discusses the importance of inflammation for immune response and its potential role in chronic diseases and organ damage. The mechanisms triggering, hindering, or resolving inflammation have been studied, but precise therapeutic interventions are not yet fully understood. The article highlights the role of cellular phenotypes, particularly neutrophils, macrophages, and platelets, in inflammation research and suggests implications for diagnostics and therapeutics.
Article
Medical Laboratory Technology
Wenhui Wang, Linlin Liu, Zhongping Ning, Lin Che, Xinming Li
Summary: This study aimed to evaluate whether the neutrophil-lymphocyte ratio (NLR) can predict poor prognosis in critically ill patients with acute myocardial infarction (AMI). The results showed that patients in the high-NLR and very high-NLR groups had higher risks of 1-year mortality, 90-day mortality, in-hospital mortality, and acute kidney injury (AKI) incidence compared to the low-NLR group. NLR is an independent risk factor for 1-year mortality, 90-day mortality, in-hospital mortality, and AKI incidence in AMI patients.
Article
Multidisciplinary Sciences
Shu-Juan Zhang, Cong-Xin Huang, Qing-Yan Zhao, He Huang, Jian Zhang
Summary: This study found that M-CSF can increase the expression of M2 macrophage and decrease the levels of M1 macrophage by regulating the P2X7R/NLRP3/IL-1 beta signal pathway, thereby inhibiting inflammation, reducing myocardial hypertrophy, apoptosis, and fibrosis.