Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
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.
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.
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.
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.
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.
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.
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.
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.
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.
