Johannes Backs

This study shows that HDAC inhibition with SAHA reduces doxorubicin-induced cardiotoxicity by modulating Topo IIb and MEF2-dependent transcription.

This study identifies FYCO1 as a regulator of autophagy that improves cardiac remodeling after myocardial infarction by enhancing autophagic flux and reducing inflammation.

This study shows that selective class IIa HDAC inhibition improves diastolic dysfunction in HFpEF without adverse effects.

The paper uses single molecule long-read sequencing to analyze transcriptomes in heart failure patients and controls, identifying novel isoforms and convergent isoform changes across different cardiomyopathy types.

This study shows that reverse cardiac remodeling is a constrained multicellular state with partial recovery of metabolic programs but persistent inflammatory-mitochondrial dysfunction, mediated by lymphatic-derived Reelin.

The paper shows that genomic G quadruplexes regulate mRNA splicing by recruiting RNA-binding proteins, with implications for cardiac function.

The paper identifies CAMK2-NR4A1 signaling as a driver of metabolic substrate switching in heart failure with reduced ejection fraction, linking it to cardiac dysfunction through glucose utilization and lipid depletion.

This study shows that somatic HDAC4-902fs mutations cause loss of HDAC4 function via nonsense-mediated mRNA decay, leading to premature ossification and early death in mice.

This study identifies CAMK2D overactivation as the cause of heart failure in RBM20 cardiomyopathy and shows pharmacological inhibition can reverse cardiac dysfunction.

The paper presents TACOMA, a web tool integrating transcriptomics and proteomics data from a TAC-induced heart failure model, revealing molecular mechanisms of cardiac remodelling and failure.

This study uses base editors and AAVMYO to correct Rbm20 mutations in cardiomyocytes, improving splicing and cardiac function in mouse models of dilated cardiomyopathy.

This study shows that phosphorylation of threonine 107 in Glo1 by CamKIIδ increases its catalytic efficiency and reduces proteasomal degradation, enhancing MG detoxification.