S. Dimmeler

The aging-induced long non-coding RNA MIRIAL controls endothelial cell and mitochondrial function

This paper identifies MIRIAL as an aging-induced lncRNA that regulates endothelial quiescence and mitochondrial function through a novel triplex mechanism.

Age-dependent RGS5 loss in pericytes induces cardiac dysfunction and fibrosis in the heart

This study shows that loss of RGS5 in pericytes with age leads to cardiac dysfunction and fibrosis by altering pericyte function and activating fibroblasts.

DNMT3A clonal hematopoiesis-driver mutations induce cardiac fibrosis by paracrine activation of fibroblasts

This study shows that DNMT3A mutations in hematopoietic cells drive cardiac fibrosis by activating fibroblasts through paracrine signaling, contributing to heart failure progression.

Ageing impairs the neuro-vascular interface in the heart

This study shows aging reduces nerve density in the left ventricle and dysregulates neuro-regulatory genes, leading to reduced heart rate variability.

Identification of novel antiviral drug candidates using an optimized SARS-CoV-2 phenotypic screening platform

This study develops a phenotypic screening platform using caspase 3/7 activity to identify antiviral compounds against SARS-CoV-2, including novel candidates and combinations.

Aging-regulated TUG1 is dispensable for endothelial cell function

This study shows that TUG1, despite high expression and conservation, does not significantly affect endothelial cell function in vitro.

Anticancer immunotherapies transition postcapillary venules into high-endothelial venules that generate TCF1+ T lymphocyte niches through a feed-forward loop

This paper shows that antiangiogenic immunotherapies convert postcapillary venules into high-endothelial venules that support TCF1+ T cell niches through a feed-forward loop involving CD8 and NK cells.

SARS-CoV-2 infects and induces cytotoxic effects in human cardiomyocytes

This study shows SARS-CoV-2 infects human cardiomyocytes, causing cytotoxicity and apoptosis, and confirms this in cardiac tissue models.

Effects of Post-Myocardial Infarction Heart Failure on the Bone Vascular Niche

This study investigates how post-myocardial infarction heart failure affects the bone vascular niche, showing age-independent loss of type H endothelium and increased inflammatory gene expression in human bone marrow endothelium.