Key result
ONO-1301MS significantly attenuated myocardial fibrosis and reduced collagen content in murine cardiac allografts undergoing chronic rejection.
Why the study?
Does ONO-1301MS prevent chronic myocardial remodeling in murine cardiac allografts?
Does ONO-1301MS prevent chronic myocardial remodeling in murine cardiac allografts?
ONO-1301MS may be an effective strategy to suppress chronic myocardial remodeling and fibrosis following cardiac transplantation based on murine models.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in murine allografts; leaves open translation to human cardiac transplant recipients.
ONO-1301MS is a compound that acts as a prostacyclin agonist with thromboxane A2 synthase inhibitory activity. We investigated the effect of ONO-1301MS on myocardial remodeling in murine cardiac allografts. The hearts of Balb/c mice were transplanted into C3H/He mice (a full allomismatch combination) to assess acute rejection or C57BL/6 hearts into B6.C-H2(‹bm12›) KhEg (a class II mismatch combination) to examine chronic rejection. ONO-1301MS did not prolong full allomismatch cardiac graft survival. Severe myocardial fibrosis with high collagen concentration was observed in untreated class II mismatch allografts on day 60. However, significantly suppressed myocardial fibrosis with less collagen synthesis was observed in the ONO-1301MS-treated group compared to the control group. ONO-1301MS could be an effective strategy to suppress chronic myocardial remodeling in cardiac transplantation.
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Suzuki et al. (2012) studied Cardiac allograft rejection. ONO-1301MS vs. Vehicle was evaluated on Myocardial fibrosis and collagen content at day 60 (p=<0.05). ONO-1301MS significantly attenuated myocardial fibrosis and reduced collagen content in murine cardiac allografts undergoing chronic rejection.
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