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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.
Human pluripotent stem cells have been shown to be important models for interrogating the molecular basis for heart disease. This review highlights the contributions of these models to our understanding of inherited arrhythmia syndromes, with a focus on integrating mechanistic and genome-wide association study data.
Acute depletion of meningeal lymphatic vessels impairs the clearance of cerebrospinal fluid and brain macromolecules. A new study by Antila et al. shows that amyloid pathology in Alzheimer’s disease is neither improved nor aggravated by genetic expansion or depletion of meningeal lymphatic vessels.
Hepatocytes are recognized as having a primary role in production and clearance of apolipoprotein B100-containing lipoproteins. A new study finds that Kupffer cells can respond to the initial atherogenic dyslipidemia and regulate levels of circulating lipoprotein.
Older men with loss of the Y chromosome are more susceptible to heart failure but the responsible genes have not been identified. A study now shows that loss of a single Y chromosome gene in bone marrow cells induces heart failure by switching cardiac macrophages from an inflammatory to a fibrogenic pattern of gene activity.
Recent analyses of observational data from 340,000 UK Biobank participants indicate that people with a higher biological age than their same-aged peers have an increased risk of developing cardiometabolic diseases. By contrast, the ability of accelerated biological aging to predict multimorbidity progression is relatively limited.
Motivated by a CRISPR screen, in vitro and in vivo studies identified an essential role for the bromodomain and extraterminal domain (BET) family member BRD4 in the differentiation of second heart field progenitors into cardiomyocytes. Single-cell transcriptomic studies showed that BRD4 deficiency affects a specific subset of cardiac progenitor cells.
Cardiometabolic multimorbidity — the coexistence of type 2 diabetes, ischemic heart disease or stroke — is a growing clinical and public health challenge. Accelerated biological aging, measured by clinical traits, provides innovative clues into subclinical prevention of cardiometabolic multimorbidity and mortality among older adults.
Myocarditis, an inflammatory heart disease, causes cardiomyocyte loss leading to heart failure. Research now shows that BMP4 is crucial for cardiac tissue homeostasis, and targeted neutralization of BMP inhibitors GREM1 and GREM2 mitigates T cell-induced myocardial inflammation and maintains cardiomyocyte integrity.
Based on the 19th Global Cardiovascular Clinical Trialists meeting, this Perspective discusses potential sources of evidence that may be used to complement explanatory phase 3 randomized clinical trials and accelerate the development of new cardiovascular medications.
The cellular microenvironment and interplay between cell types are essential for cardiac renewal. Combined single-cell and single-nucleus sequencing, spatial transcriptomics and loss-of-function experiments in constitutively YAP-expressing infarcted hearts reveal a cellular triad and complement signaling that evoke renewal of heart muscle.
In coronary artery disease, the transition from an apparently stable state to a life-threatening acute cardiac event is difficult to predict. As such, a recent study applied proteomic and metabolomic approaches to discover new biomarkers that signal imminent myocardial infarction.
Defects in platelet adhesion at sites of injury can lead to excessive bleeding. A study by Gandhi et al. investigates a new bispecific antibody as a possible therapy to prevent bleeding in patients with inherited defects in platelet adhesion.
Myocardial infarction causes endoplasmic reticulum (ER) stress, thereby triggering the release of a set of poorly defined growth factors. A study shows that the growth factor CRELD2 is secreted in response to ER stress and is required for preserving heart function after myocardial infarction in mice.
Cerebrospinal fluid is now thought to drain through lymphatics instead of veins, but the routes the fluid takes from the subarachnoid space to cervical lymph nodes are unclear. Using advanced imaging, a recent study provides unprecedented anatomical details of lymphatic vessels draining cerebrospinal fluid along the nasopharynx.
