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In lung tissues of pulmonary hypertension rodent models, B cell activation and immunoglobulin E (IgE) production lead to mast cell activation and release of the cytokines IL-6 and IL-13, which result in remodeling of vascular smooth muscle cells. Blockade of IgE with omalizumab, a clinically approved monoclonal antibody against IgE, alleviated the progression of experimental pulmonary hypertension.
Transiently inducing proliferation of adult cardiomyocytes is a long-sought goal in the cardiac regeneration field. A new study shows that genetic deletion of calcineurin B1 and treatment with FK506 (tacrolimus, an FDA-approved inhibitor of calcineurin) induce cardiomyocyte proliferation in adult mice.
Viral infections and cardiovascular disease (CVD) share a two-way connection: viral infection can raise CVD risk, and people with CVD are more prone to severe viral infection. Zhao et al. now detail a molecular mechanism whereby macrophages from patients with CVD inhibit antiviral T cell responses via immune checkpoint activation.
A mouse model of spontaneous arrhythmia in awake mice enables researchers to study how immune cells contribute to this process. The authors find opposing effects of the immune compartment, with neutrophils favoring arrhythmias by increasing oxidative stress and macrophages protecting against it via their phagocytic activity.
Libby and Tokgözoğlu discuss the management of atherogenic lipoproteins, notably low-density lipoprotein, with an emphasis on the role of strategies that target PCSK9.
The stretch-activated ion channel Piezo1 senses biomechanical stress and provides calcium for transcriptional activation and cardiac growth. In turn, the high amplitude of calcium determines specific signaling through the CaMKII–HDAC–MEF2 pathway as opposed to the calcineurin–NFAT pathway.
In a prospective experimental observational study of 18 individuals with severe, recurrent extracranial arteriovenous malformations, thalidomide was effective in reducing pain, healing ulceration, stopping bleeding and resolving cardiac failure.
A prospective observational case-report study now shows that thalidomide can be a well-tolerated, efficacious treatment for complications such as pain, bleeding and ulceration from extracranial arteriovenous malformation.
Clonal hematopoiesis is a risk factor for hematological cancers, cardiovascular diseases and death. Two papers now use new experimental and mathematical tools to quantify changes in the clonal composition of human blood over time, and the results have implications for the risk of cardiovascular diseases.
Rupture or dissection of the aorta is often fatal. Tcheandjieu and colleagues now identify key pathways underlying aortic dilatation, a common prelude to acute aortic events, and assess the utility of a polygenic risk score to identify those at highest risk of aortic death in whom prophylactic surgical repair may be beneficial.
Blood vessels are thought to form either by de novo vasculogenesis or by angiogenesis from pre-existing blood vessels. Research now finds that anal fin blood vessels form by endothelial transdifferentiation from lymphatic vessels.
Elucidation of the mechanisms that drive tumor resistance to anti-angiogenic therapies is expected to improve treatment options. This report shows that endothelial apelin signaling promotes the migration of distant venous endothelial cells toward the tumor progenitor cell niche to support vessel expansion and sustain a normoxic microenvironment, and that it does so independently of vascular endothelial growth factor A.
Fibroblast growth factor homologous factors (FHFs) are an auxiliary subunit of the cardiac voltage-gated sodium channel. We found that FHFs can inhibit the arrhythmogenic late sodium current (INa,L) in an isoform-specific manner, and engineered an FHF-based cell-penetrating peptide that acts as an inhibitor of INa,L and opens avenues for developing future therapeutics.
Using a quantitative statistical approach, we created a 3D atlas of embryonic cardiac morphogenesis from a collection of mouse specimens. The atlas includes the average shape of tissue geometry over time and its range of variability, and it enabled us to identify the onset of cardiac left–right asymmetry.
Dysregulation of voltage-gated cardiac Na channels can be arrhythmogenic. A new study shows that splice variants of fibroblast growth factor homologous factors (FHFs) can either promote or suppress arrhythmogenic late Na current, and the peptide inhibitor FixR could represent a therapeutic strategy to treat cardiac arrhythmias.
Blood vascular leakage in conjunction with stroke causes edema and a worsened outcome. Through augmented and selective tyrosine phosphatase activity, endothelial junctions can be sealed, resulting in reduced stroke volume and improved survival.
Apelin is a multifunctional peptide that stimulates angiogenesis in a VEGF-A-dependent manner. A study now shows that apelin produced by intestinal endothelium drives VEGF-A-independent angiogenesis in intestinal crypts and is needed for the homeostasis of crypt-resident stem or progenitor cells.
In this Review, the authors provide an overview of the clinical and experimental studies supporting the notion that allergic asthma and associated allergies affect the prevalence, incidence and progression of cardiovascular disease.
Ziad Mallat and Christoph Binder discuss the current knowledge of the adaptive immune response in the immuno-cardiovascular unit, in health and in atherosclerotic disease.
Loss of transcription factor SMAD3 changes the smooth muscle cell (SMC) to a unique remodeling SMC phenotype and points to a potential role for SMAD3 in the inhibition of macrophage recruitment and outward remodeling of the aortic wall.
