Injectable human recombinant collagen matrices limit adverse remodeling and improve cardiac function after myocardial infarction.
Sarah McLaughlinBrian McNeillJames PodrebaracKatsuhiro HosoyamaVeronika SedlakovaGregory CronDavid SmythRichard SeymourKeshav GoelWenbin LiangKatey J RaynerMarc RuelErik J SuuronenEmilio I AlarconPublished in: Nature communications (2019)
Despite the success of current therapies for acute myocardial infarction (MI), many patients still develop adverse cardiac remodeling and heart failure. With the growing prevalence of heart failure, a new therapy is needed that can prevent remodeling and support tissue repair. Herein, we report on injectable recombinant human collagen type I (rHCI) and type III (rHCIII) matrices for treating MI. Injecting rHCI or rHCIII matrices in mice during the late proliferative phase post-MI restores the myocardium's mechanical properties and reduces scar size, but only the rHCI matrix maintains remote wall thickness and prevents heart enlargement. rHCI treatment increases cardiomyocyte and capillary numbers in the border zone and the presence of pro-wound healing macrophages in the ischemic area, while reducing the overall recruitment of bone marrow monocytes. Our findings show functional recovery post-MI using rHCI by promoting a healing environment, cardiomyocyte survival, and less pathological remodeling of the myocardium.
Keyphrases
- heart failure
- wound healing
- left ventricular
- acute myocardial infarction
- bone marrow
- type iii
- recombinant human
- endothelial cells
- end stage renal disease
- atrial fibrillation
- tissue engineering
- newly diagnosed
- ejection fraction
- mesenchymal stem cells
- risk factors
- percutaneous coronary intervention
- hyaluronic acid
- stem cells
- type diabetes
- optical coherence tomography
- emergency department
- high glucose
- acute coronary syndrome
- dendritic cells
- immune response
- peripheral blood
- adverse drug
- cell therapy
- replacement therapy
- electronic health record
- combination therapy
- skeletal muscle
- drug induced