HBI-8000 improves heart failure with preserved ejection fraction via the TGF- β1/MAPK signalling pathway

In conclusion, our data suggest that HBI-8000 inhibits fibrosis by modulating the TGF-β1/MAPK pathway thereby improving HFpEF. Therefore, HBI-8000 may become a new hope for the treatment of HFpEF patients.PMID:38509729 | DOI:10.1111/jcmm.18238
Source: J Cell Mol Med - Category: Molecular Biology Authors: Source Type: research