Why the study?
Right heart failure and RV remodeling are the main cause of mortality in pulmonary hypertension, and ApoA5 has multifunction in several target organs.
Does ApoA5 overexpression protect against right ventricular failure and fibrosis secondary to pulmonary hypertension?
Does ApoA5 overexpression protect against right ventricular failure and fibrosis secondary to pulmonary hypertension?
ApoA5 overexpression protects against right ventricular failure and fibrosis in pulmonary hypertension models by inhibiting the FAK-JNK-Smad3 pathway.
ApoA5 may protect RV in PH; hypothesis-generating and requires clinical validation before therapeutic consideration.
Right heart failure and right ventricular (RV) remodeling were the main reason for mortality of pulmonary hypertension (PH) patients. Apolipoprotein AV (ApoA5) is a key regulator of plasma triglyceride and have multifunction in several target organs. We detected decreased ApoA5 in serum of patients with PH and both in serum and RV of monocrotaline-induced PH model. Exogenously, overexpression ApoA5 by adenovirus showed protective effects on RV failure and RV fibrosis secondary to PH. In addition, in vitro experiments showed ApoA5 attenuated the activation of fibroblast induced by transforming growth factor β1 and synthesis and secretion of extracellular matrix by inhibiting focal adhesion kinase-c-Jun N-terminal kinase-Smad3 pathway. Finally, we suggest that ApoA5 may potentially be a pivotal target for RV failure and fibrosis secondary of PH.
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Chen et al. (2020) studied this question.
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