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An integrative approach, combining genetic mouse and large-scale human genetics studies, was used to reveal a novel role for the Bcl-2 protein Bid in maintenance of mitochondrial function that alters susceptibility to myocardial infarction.

Elucidating widespread and tissue-specific biological process alterations after myocardial infaction in metabolically active tissues using systems biology approaches.

β₃-AR signalling via cGMP in cardiomyocytes is regulated via phosphodiesterase 2 and 5 degradation, it is potentially cardioprotective, but dysregulated in heart failure through signal redistribution and higher phosphodiesterase activity.

Cardiac fibroblast reduction is well-tolerated and demonstrates beneficial outcomes after heart injury.

Lymphangiogenic therapy VEGFCc156s improved angiotensin-II-induced impairments in heart function via novel mechanisms, which include transcriptional responses to alleviate inflammation and cardiac fibrosis, and systemic responses to ameliorate hypertension.

Research on heart tube assembly using zebrafish reveals a pivotal role for intrinsic Pdgfra–PI3K signaling in steering the movement of the myocardium and polarizing myocardial cell protrusions.

Cardiac lymphatic vessels of heterogeneous origins and molecular signatures support cardiac growth and regeneration.

Mitophagy regulates mitochondrial quality and mediates extensive mitochondrial degradation in (patho-)physiological settings and is one of the key components of hypoxic preconditioning which protects the heart from ischemia/reperfusion injury.

Human cardiac fibroblasts regulate their cellular responses according to the combination of multiple environmental stimuli namely oxygen changes and mechanical signals.