CardioAtlas: deciphering the single-cell transcriptome landscape in cardiovascular tissues and diseases.

Increasing scRNA-seq data in cardiovascular research have substantially improved our knowledge on the development of the cardiovascular system and the mechanisms underlying cardiovascular diseases. However, the single-cell transcriptome datasets were dispersed in literature and no resource for cardiovascular systems and diseases. Here, we constructed an organized resource CardioAtlas, which provides comprehensive analysis results for > 1,929,000 cells in 27 human data sets and > 1,088,000 cells in 39 mouse data sets.

Acetylcytidine modification of Amotl1 by N-acetyltransferase 10 contributes to cardiac fibrotic expansion in mice after myocardial infarction.

Cardiac fibrosis is a pathological scarring process that impairs cardiac function. N-acetyltransferase 10 (Nat10) is recently identified as the key enzyme for the N4-acetylcytidine (ac4C) modification of mRNAs. In this study, we investigated the role of Nat10 in cardiac fibrosis following myocardial infarction (MI) and the related mechanisms.

LncRNA-LncDACH1 mediated phenotypic switching of smooth muscle cells during neointimal hyperplasia in male arteriovenous fistulas.

Arteriovenous fistulas (AVFs) are the most common vascular access points for hemodialysis (HD), but they have a high incidence of postoperative dysfunction, mainly due to excessive neointimal hyperplasia (NIH). Our previous studies have revealed a highly conserved LncRNA-LncDACH1 as an important regulator of cardiomyocyte and fibroblast proliferation. Herein, we find that LncDACH1 regulates NIH in AVF in male mice with conditional knockout of smooth muscle cell-specific LncDACH1 and in male mice model of AVF with LncDACH1 overexpression by adeno-associated virus.

N-Acetyltransferase 10 represses Uqcr11 and Uqcrb independently of ac4C modification to promote heart regeneration.

Translational control is crucial for protein production in various biological contexts. Here, we use Ribo-seq and RNA-seq to show that genes related to oxidative phosphorylation are translationally downregulated during heart regeneration. We find that Nat10 regulates the expression of Uqcr11 and Uqcrb mRNAs in mouse and human cardiomyocytes.

Cannabidiol represses miR-143 to promote cardiomyocyte proliferation and heart regeneration after myocardial infarction.

Mammalian heart is capable to regenerate almost completely early after birth through endogenous cardiomyocyte proliferation. However, this regenerative capacity diminishes gradually with growth and is nearly lost in adulthood. Cannabidiol (CBD) is a major component of cannabis and has various biological activities to regulate oxidative stress, fibrosis, inflammation, and cell death.

Long non-coding RNA regulates cardiomyocyte differentiation through H2A.Z-mediated LHX1 transcriptional activation.

Long non-coding RNAs (lncRNAs) play widespread roles in various processes. However, there is still limited understanding of the precise mechanisms through which they regulate early stage cardiomyocyte differentiation. In this study, we identified a specific lncRNA called , which is transcribed from a bidirectional promoter of LIM Homeobox 1 (LHX1) gene.

Prophylactic rivaroxaban in the early post-discharge period reduces the rates of hospitalization for atrial fibrillation and incidence of sudden cardiac death during long-term follow-up in hospitalized COVID-19 survivors.

While acute Coronavirus disease 2019 (COVID-19) affects the cardiovascular (CV) system according to recent data, an increased CV risk has been reported also during long-term follow-up (FU). In addition to other CV pathologies in COVID-19 survivors, an enhanced risk for arrhythmic events and sudden cardiac death (SCD) has been observed. While recommendations on post-discharge thromboprophylaxis are conflicting in this population, prophylactic short-term rivaroxaban therapy after hospital discharge showed promising results.

Early antithrombotic post-discharge therapy using prophylactic DOAC or dipyridamole improves long-term survival and cardiovascular outcomes in hospitalized COVID-19 survivors.

Introduction: Cardiovascular events are common in COVID-19. While the use of anticoagulation during hospitalization has been established in current guidelines, recommendations regarding antithrombotic therapy in the post-discharge period are conflicting.

Methods: To investigate this issue, we conducted a retrospective follow-up (393 ± 87 days) of 1,746 consecutive patients, hospitalized with and surviving COVID-19 pneumonia at a single tertiary medical center between April and December 2020.

Cardiovascular Biomarkers for Prediction of in-hospital and 1-Year Post-discharge Mortality in Patients With COVID-19 Pneumonia.

Aims: While COVID-19 affects the cardiovascular system, the potential clinical impact of cardiovascular biomarkers on predicting outcomes in COVID-19 patients is still unknown. Therefore, to investigate this issue we analyzed the prognostic potential of cardiac biomarkers on in-hospital and long-term post-discharge mortality of patients with COVID-19 pneumonia.

Methods: Serum soluble ST2, VCAM-1, and hs-TnI were evaluated upon admission in 280 consecutive patients hospitalized with COVID-19-associated pneumonia in a single, tertiary care center.

Transcription factor Meis1 act as a new regulator of ischemic arrhythmias in mice.

Introduction: The principal voltage-gated Na channel, Na1.5 governs heart excitability and conduction. Na1.

Photobiomodulation Drives MiR-136-5p Expression to Promote Injury Repair after Myocardial Infarction.

Photobiomodulation (PBM) has emerged as an alternative therapy involved in modulating a variety of biological effects. In this study, we verified whether PBM can affect cardiac physiological activity in mice through noninvasive irradiation using light-emitting diodes at a wavelength of 630 nm (LED-Red). We found that the PBM involved in regulating the repair of injured myocardium is wavelength-limited.

Mettl3 deficiency leads to the upregulation of Cav1.2 and increases arrhythmia susceptibility in mice.

Methyltransferase-like 3 (Mettl3) is a component of methyltransferase complex that mediates mA modification of RNAs, and participates in multiple biological processes. However, the role of Mettl3 in cardiac electrophysiology remains unknown. This study aims to explore the ventricular arrhythmia susceptibility of Mettl3 mice and the underlying mechanisms.

Targeting cardiomyocyte proliferation as a key approach of promoting heart repair after injury.

Cardiovascular diseases such as myocardial infarction (MI) is a major contributor to human mortality and morbidity. The mammalian adult heart almost loses its plasticity to appreciably regenerate new cardiomyocytes after injuries, such as MI and heart failure. The neonatal heart exhibits robust proliferative capacity when exposed to varying forms of myocardial damage.

J-waves in acute COVID-19: A novel disease characteristic and predictor of mortality?

Background: J-waves represent a common finding in routine ECGs (5-6%) and are closely linked to ventricular tachycardias. While arrhythmias and non-specific ECG alterations are a frequent finding in COVID-19, an analysis of J-wave incidence in acute COVID-19 is lacking.

Methods: A total of 386 patients consecutively, hospitalized due to acute COVID-19 pneumonia were included in this retrospective analysis.

ALKBH5-mediated mA mRNA methylation governs human embryonic stem cell cardiac commitment.

N6-methyladenosine (mA), as the most abundant modification of mammalian messenger RNAs, is essential for tissue development and pathogenesis. However, the biological significance of mA methylation in cardiac differentiation and development remains largely unknown. Here, we identify that the downregulation of mA demethylase ALKBH5 is responsible for the increase of mA methylation and cardiomyocyte fate determination of human embryonic stem cells (hESCs) from mesoderm cells (MESs).

Loss of mA methyltransferase METTL3 promotes heart regeneration and repair after myocardial injury.

Aims: N6-Methyladenosine (mA), one of the important epigenitic modifications, is very commom in messenger RNAs (mRNAs) of eukaryotes, and has been involved in various diseases. However, the role of mA modification in heart regeneration after injury remains unclear. The study was conducted to investigate whether targeting methyltransferase-like 3 (METTL3) could replenish the loss of cardiomyocytes (CMs) and improve cardiac function after myocardial infarction (MI).

Photobiomodulation Regulation as One Promising Therapeutic Approach for Myocardial Infarction.

Myocardial infarction refers to myocardial necrosis caused by acute or persistent coronary ischemia and hypoxia. It is considered to be one of the significant crises threatening human health in the world. Following myocardial infarction, collagen gradually replaces the original tissue due to the loss of many cardiomyocytes, myocardial contractile function decreases, and myocardial fibrosis eventually leads to heart failure.

Blue LED causes autophagic cell death in human osteosarcoma by increasing ROS generation and dephosphorylating EGFR.

Osteosarcoma (OS) is the most common primary malignant bone tumour in adolescence. Lately, light-emitting diodes (LED)-based therapy has emerged as a new promising approach for several diseases. However, it remains unknown in human OS.

ACE2 as a Key Target for Treatment of COVID-19 Related Cardiovascular Diseases: Current Progress and Prospect.

ACE2 has long been known as an injury protective protein, which can protect against a variety of organ damage such as the heart, liver, kidney, and lung. Especially in cardiovascular diseases, as a negative regulator of RAAS, ACE2 is an extremely important protective factor that mainly plays a role by converting Ang II to Ang-(1-7). Nevertheless, with the recent outbreak of COVID-19, it is exposed that another identity of ACE2 is the entry receptor for SARS-CoV-2, which previously serves as the entry receptor for SARS.