ghazaleh asgharnezhad

Lots of people die from heart failure (HF) because of fibrosis formation. As injured myocytes deregulated MMP-2, MMP-4, TIMP-2, Ang, plasma renin activity  (PRA), and ACE leading to fibrosis, their regulation can improve HF. One of the most effective treatments for heart failure is the use of hAMSCs-CM, which has been shown to improve heart function and reduce symptoms. The study innovation was the investigation of the in vivo mode of action of hAMSCs-CM on HF fibrosis focusing on the mentioned proteins for the first time. We expected that this study partly fill the scientific gap in HF treatment. Frothy rats were divided into 4 groups; Control, HF, culture medium, and CM. To induce HF, isoproterenol (ISO) was injected into all animals except for the control. CM were injected into the CM group and the culture medium group received culture medium. Then, cardiac functions were measured using echocardiography and serum fibrosis was evaluated by ELISA. HF model showed decreased MMP-2, MMP-4, Ang, PRA, and ACE and increased TIMP-2, whereas hAMSCs-CM therapy reversed them compared with controls. Our result has partially filled the HF treatment’s gap as hAMSCs-CM improved cardiac function and reduced cardiac fibrosis and the serum fibrogenic proteins.