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Doxorubicin treatment is a mainstay of cancer therapy but causes potent cardiotoxicity that exposes cancer survivors to the risk of heart failure. A study now identifies CD8+ T cells of the adaptive immune system as major culprits in the development of doxorubicin-induced cardiomyopathy and heart failure.
Myocardial infarction can damage the heart muscle and lead to heart failure. Research on recovery typically focuses on infiltrating immune cells, damaged cardiomyocytes, over-stimulated fibroblasts and changes in vasculature. Haykin et al. now describe a multi-organ circuit linking these entities, including the brain and liver, in the repair process.
In response to high fluid shear stress, KLF2-mediated induction of the BMP inhibitor BMPER improves outward arterial remodeling. This knowledge is translated into a preclinical model showing that BMP9 and BMP10 neutralizing antibodies enhance flow recovery and arterialization in ischemia in diabetic mice.
Myofibroblast activation requires nuclear translocation of ATP citrate lyase (ACLY) that triggers chromatin remodeling and the induction of fibrosis-associated genes. ACLY inhibition prevents myofibroblast conversion and causes de-differentiation of myofibroblasts to fibroblasts, indicating a potential therapeutic approach for heart failure.
We describe the regenerative senescence signature of the injured mouse heart using proteomics and single-cell RNA sequencing. We report that transient senescence is required for neonatal mouse heart regeneration and for agrin-mediated cardiac repair in adult mice and provide insights into the essential role of Egr1 in senescence and regeneration.
Liver sinusoidal endothelial cells have small pores called fenestrae that allow bidirectional exchange of substrates such as lipids between hepatocytes and blood. New work reveals molecular pathways linking hyperlipidemia to these cells’ loss of fenestrae as a starting point for metabolic dysfunction-associated steatotic liver disease.
Rare and common variants in HTRA1 are associated with ischemic stroke. Research now sheds light on the underlying genetic architecture and suggests a vasculopathy with a broader phenotypic spectrum. Lower HTRA1 protease activity and circulating levels both predict an increased risk of ischemic stroke and coronary artery disease.
Carpenter and Maryanovich explore how hematopoietic homeostasis, governed by local niche and systemic mechanisms, is impacted by environmental and immune stressors like stress, sleep patterns, aging and inflammation and examine the implications for cardiovascular diseases.
We discover a function of innate immune cells that is important for healing injury: macrophages adopt mural cell roles that are important for restoring blood vessel function and perfusion.
Fernandez-Patron et al. propose a unifying framework explaining how diverse risk factors such as hypertension, obesity and diabetes lead pathogenesis and progression of heart failure.
A study describes the role of the ACTN2 enhancer in myocardial maturation, highlighting its relevance in regulating structural, functional and metabolic dynamics in the heart. These findings offer insights that may advance our understanding of cardiovascular disease.
Fleetwood et al. review the role of immune cell dysfunction and inflammation in cardiovascular diseases. Their Review explores immune cell metabolic reprogramming in response to environmental cues, offering insights into potential therapeutic strategies for cardiovascular diseases.
Eschenhagen and Weinberger provide a concise and comprehensive overview of the perspectives and challenges of heart repair with pluripotent stem cell-derived cardiomyocytes.
By dissecting the cell composition and function of arterial grafts derived from the internal thoracic, radial and right gastroepiploic arteries, we identified factors that might promote patency rates of arterial grafts, including combating lipid deposition, disturbances in wall shear stress, smooth muscle cell proliferation, fibrosis and spasm.
The mechanisms by which stroke and myocardial infarction trigger lymphocyte loss remain poorly defined. This study shows that the release of neutrophil extracellular traps (NETs) after stroke and myocardial infarction triggers B cell apoptosis and reduces the number of IgA-producing plasma cells. Therapeutic targeting of NETs is immunoprotective in mice and humans.
The eye and the brain are both recognized as immune-privileged sites. Research now indicates that responses in the eye mirror those in the central nervous system (CNS), offering major implications for the treatment of CNS cancers and infections.
On 21–23 September 2023, the Immuno-Cardiology Symposium was hosted by the Leducq Foundation Networks of Excellence Program (The Inflammatory-Fibrosis Axis in Adverse LV Remodeling: translating mechanisms into new diagnostics and therapeutics) at The Jackson Laboratory in Bar Harbor, Maine. The symposium highlighted recent advances in the basic science of dysregulated immune system activation and fibrosis in response to cardiac injury.
Adult hearts have inherently limited regenerative capabilities, such that injury results in lasting damage. The situation is different in neonatal mouse hearts, however, where a new study reveals a role for the immunomodulatory PD-1–PD-L1 pathway in regulating regeneration after injury.
High-throughput sequencing technologies have revolutionized the study of transcription across cell types and many biological phenomena. Brash et al. have developed a resource based on 240 endothelial bulk RNA-sequencing datasets that uses machine learning to predict whether a gene is the product of leaky or active transcription.
