摘要
In a recent study published in Nature Genetics,1 Han and colleagues employed a dual genetic lineage tracing approach in combination with a model of heart failure(HF)to identify a key sub-population of endocardium-derived fibroblasts,which gives rise to excessive myofibroblast formation in a Wnt pathway-mediated manner and contributes to cardiac fibrosis.1 The identified fibroblast sub-population and Wnt signaling pathway could be novel targets for the therapy of HF.Improvements in risk management and cardiovascular inter-vention have significantly reduced age-specific cardiovascular disease-related mortality.In contrast,the rate of HF-related hospitalisations has increased over the past decades and HF is a disease with highest social and economic cost in industrialized countries.HF is defined as impairment of the heart’s blood pumping function and its severity is assessed based on ejection fraction.HF often occurs after myocardial infarction(MI),with infarct size and quality of ventricular remodeling after MI influencing ventricular dysfunctions.Causes of HF also include hypertension,atrial fibrillation,and cardiomyopathies(Fig.1).Especially elderly patients with recurrent MI and comorbidities are increasingly presenting with signs of HF.
基金
J.B.received funding from Deutsche Forschungsgemeinschaft(DFG)grants DFG-SFB1123-A3,BE 1977/14-1
the Munich Cluster for Systems Neurology(DFG,EXC 2145 SyNergy-ID 390857198)
well as from the German Center for Cardiovascular Diseases(DZHK)
partner site Munich Heart Alliance(grant DZHK B 20-004 Extern-81×2600258)
Y.A.acknowledges support from DFG grant SFB1123-B3 and AS 575/1-1 and C.S.received funding from DFG grant STO 1099/8-1.
