Image courtesy of  Dr. Derek Sung, University of Pennsylvania

Read our November issue

A new mouse model for gene targeting in VSMCs, the spatiotemporal transcriptomics of the border zone, the digoxin chronotherapy for treatment of the myocardial ischemia-reperfusion injury, and more!

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  • Komuro et al. performed an integrative analysis of single-nucleus RNA sequencing and spatial transcriptome analysis of the injured heart to map cellular and molecular changes across topographical domains relative to the site of injury, and they identify that mechano-sensing genes at the border zone act as adaptive regulators of left ventricular remodeling.

    • Shintaro Yamada
    • Toshiyuki Ko
    • Issei Komuro
    Article Open Access
  • Using single-cell/single-nucleus RNA sequencing and spatial transcriptomic analysis, Calcagno and Taghdiri et al. define the ischemic border zone—the area between the poorly perfused infarct area and the remote zones of the heart—based on the cardiomyocyte transcriptomes. The transcriptional border zone emerges within an hour of the ischemic injury and can be observed in response to any injury that causes loss of neighboring cells and mechanical destabilization, including the trauma induced with a fine needle.

    • D. M. Calcagno
    • N. Taghdiri
    • K. R. King
    Article
  • Papa et al. show that phosphorylation by PKA of four residues in Rad, a calcium channel inhibitor, is required to mediate the β-adrenergic-induced increase in calcium current and contractile force. Additionally, Rad-phosphosite-mutant mice showed reduced basal heart rate and contractility. Conversely, expression of mutant calcium channel unable to bind wild-type or phosphosite-mutant Rad was sufficient to enhance basal calcium influx and contractility, independently of β-adrenergic stimulation.

    • Arianne Papa
    • Sergey I. Zakharov
    • Steven O. Marx
    Article Open Access
  • Using various mouse models, human plaque data and isolated B cells combined with state-of-the-art imaging and transcriptomic analysis, the authors show that the G-protein-coupled orphan receptor GPR55 regulates B cell activation and plasma cell differentiation during hypercholesterolemia, which crucially affects atherosclerosis.

    • Raquel Guillamat-Prats
    • Daniel Hering
    • Sabine Steffens
    Article Open Access
  • Warthi et al. generated an alpha 8 integrin-cre driver that enables gene targeting preferentially in vascular smooth muscle cells (SMCs) and showed in a proof-of-principle study, that using the Itga8-CreERT2 knock-in mouse for selective ablation of the Srf gene caused vascular defects but not a lethal visceral myopathy observed in an SMC-specific Myh11-CreERT2-driven Srf loss.

    • Ganesh Warthi
    • Jessica L. Faulkner
    • Joseph M. Miano
    Technical Report
  • Using different genetic mice models, Sung et al. show that VEGF-C/VEGFR3 signaling is required for sinusoidal vascular growth in the fetal liver and bone marrow. CDH5 (VE-cadherin) negatively regulates VEGF-C/VEGFR3 signaling and sinusoidal and lymphatic growth. Loss of CDH5 enables growth of sinusoidal and lymphatic vessels in the absence of VEGFR3 signaling through VEGF-C/VEGFR2 signaling.

    • Derek C. Sung
    • Mei Chen
    • Mark L. Kahn
    Article
  • Although cardiac arrhythmias have been observed and described during and after SARS-CoV-2 infection, rigorous studies designed to untangle the complex relationship between this proinflammatory illness and arrhythmogenesis are limited. Despite a pervasive opinion to the contrary, there is presently no definitive data to establish a causal, viral-specific association between COVID-19 and incident arrhythmia.

    • Thomas A. Dewland
    • Gregory M. Marcus
    Comment
  • In the COVID-19 aftermath, academia experiences an unprecedented drought of postdoctoral researchers. The new generation of scientists refuses to face the low odds of starting their own labs in a competitive arena that does not align with their work–life balance needs. We discuss the possible reasons and potential measures needed to sustain talented and passionate early career researchers in academia.

    • Konstantinos Drosatos
    • Georgia Fousteri
    Comment
  • Studies of the genetic architecture of cardiovascular disease once focused on heritable germline factors. Newer work has shed light on the role of somatic mutations in blood cells. These mechanistic and multi-omics studies, along with phenotypic analyses, offer the prospect of new precision cardiovascular medicine paradigms.

    • Tetsushi Nakao
    • Pradeep Natarajan
    Comment
  • The REVIVED trial provides critical evidence on the management of patients with ischemic left ventricular dysfunction, highlighting the importance of optimal medical therapy. At the same time, it is another reminder of the fact that we are far from reaching adequate representation of women in cardiovascular disease trials.

    • Roxana Mehran
    • Birgit Vogel
    Comment