A5004154659- Cardiac Fibrosis and Remodeling
- Immune cells in cancer
- Viral Infections and Immunology Research
- Cardiomyopathy and Myosin Studies
- Cardiac Structural Anomalies and Repair
- Atherosclerosis and Cardiovascular Diseases
- Transplantation: Methods and Outcomes
- Mechanical Circulatory Support Devices
- Signaling Pathways in Disease
- Congenital heart defects research
- Renal Transplantation Outcomes and Treatments
- Tissue Engineering and Regenerative Medicine
- Single-cell and spatial transcriptomics
- Cardiovascular Effects of Exercise
- Cardiovascular Function and Risk Factors
- Cancer Immunotherapy and Biomarkers
- Bioinformatics and Genomic Networks
- Neuroinflammation and Neurodegeneration Mechanisms
- Health, Environment, Cognitive Aging
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Peptidase Inhibition and Analysis
- SARS-CoV-2 and COVID-19 Research
- Vagus Nerve Stimulation Research
- Organ Transplantation Techniques and Outcomes
- Cardiac Ischemia and Reperfusion
Washington University in St. Louis
2016-2025
University of Missouri–St. Louis
2024
Cardiovascular Research Center
2014-2023
Barnes-Jewish Hospital
2013-2021
University of Toronto
2021
Health Net
2016
John Radcliffe Hospital
2016
University Health Network
2016
Toronto General Hospital
2016
Center for Systems Biology
2016
Significance This study addresses a fundamentally important and widely debated issue in the field of inflammation, which is why inflammation can be simultaneously deleterious after injury yet essential for tissue repair. Recently, an new paradigm has emerged macrophage field: Organs are replete with resident macrophages embryonic origin, distinct from monocyte-derived macrophages. In this article, we use model cardiac show that populations derived adult lineages determinants repair...
Recent advancements have brought to light the origins, complexity, and functions of tissue-resident macrophages. However, in context tissue injury or disease, large numbers monocytes infiltrate heart are thought contribute adverse remodeling failure pathogenesis. Little is understood about diversity monocyte-derived macrophages recruited after myocardial injury, including mechanisms that regulate monocyte recruitment fate specification.We sought test hypothesis distinct subsets CCR2- (C-C...
Nonapoptotic forms of cell death can trigger sterile inflammation through the release damage-associated molecular patterns, which are recognized by innate immune receptors. However, despite years investigation, mechanisms that initiate inflammatory responses after heart transplantation remain elusive. Here, we demonstrate ferrostatin-1 (Fer-1), a specific inhibitor ferroptosis, decreases levels pro-ferroptotic hydroperoxy-arachidonoyl-phosphatidylethanolamine, reduces cardiomyocyte death,...
Macrophages reside in the healthy myocardium, participate ischemic heart disease, and modulate myocardial infarction (MI) healing. Their origin roles post-MI remodeling of nonischemic remote however, remain unclear.This study investigated number, origin, phenotype, function cardiac macrophages residing myocardium mice with chronic failure after coronary ligation.Eight weeks post MI, fate mapping flow cytometry revealed that a 2.9-fold increase results from both increased local macrophage...
Rationale: It is now recognized that macrophages residing within developing and adult tissues are derived from diverse progenitors including those of embryonic origin. Although the functions in organisms well studied, during organ development remain largely undefined. Moreover, it unclear whether distinct macrophage lineages have differing functions. Objective: To address these issues, we investigated subsets resident heart, an replete with embryonic-derived macrophages. Methods Results:...
Heart failure represents a major cause of morbidity and mortality worldwide. Single-cell transcriptomics have revolutionized our understanding cell composition associated gene expression. Through integrated analysis single-cell single-nucleus RNA-sequencing data generated from 27 healthy donors 18 individuals with dilated cardiomyopathy, here we define the failing human heart. We identify cell-specific transcriptional signatures age heart reveal emergence disease-associated states. Notably,...
There is ongoing debate as to whether cardiac complications of coronavirus disease-2019 (COVID-19) result from myocardial viral infection or are secondary systemic inflammation and/or thrombosis. We provide evidence that cardiomyocytes infected in patients with COVID-19 myocarditis and susceptible severe acute respiratory syndrome 2. establish an engineered heart tissue model pathology, define mechanisms pathogenesis, demonstrate cardiomyocyte 2 results contractile deficits, cytokine...
Recent studies have established that CCR2 (C-C chemokine receptor type 2) marks proinflammatory subsets of monocytes, macrophages, and dendritic cells contribute to adverse left ventricle (LV) remodeling heart failure progression. Elucidation the effector mechanisms mediate effects
Immune checkpoint inhibitors (ICIs), antibodies targeting PD-1 (programmed cell death protein 1)/PD-L1 death-ligand 1) or CTLA4 (cytotoxic T-lymphocyte-associated 4), have revolutionized cancer management but are associated with devastating immune-related adverse events including myocarditis. The main risk factor for ICI myocarditis is the use of combination and inhibition. often fulminant pathologically characterized by myocardial infiltration T lymphocytes macrophages. Although much has...
Microglia, resident macrophages of the CNS, are essential to brain development, homeostasis, and disease. Microglial activation proliferation hallmarks many CNS diseases, including neuropathic pain. However, molecular mechanisms that govern spinal neuroimmune axis in setting pain remain incompletely understood. Here, we show genetic ablation or pharmacological blockade transient receptor potential vanilloid type 4 (TRPV4) markedly attenuated pain-like behaviors a mouse model spared nerve...