(Letter to the Editor) Response to: protective role of peroxiredoxin-4 in heart failure.

Natalia López-Andrés
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Abstract

We thank Ahmed et al. for their letter regarding our study 'Galectin-3 down-regulates antioxidant peroxiredoxin-4 in human cardiac fibroblasts' [1]. As emphasized by Ahmed et al., Prx-4 levels decrease [2] whereas MFN-2, OPA-1 and PGC-1α levels increase [3] in dilated cardiomyopathy (DCM). Moreover, Gal-3 expression is also increased in DCM [4]. In our study, we showed in vitro that Gal-3 decreased Prx-4 without modifying MFN-2 or PGC-1α levels in human cardiac fibroblasts. Although cardiac Prx-4 decrease could be a direct consequence of Gal-3 effects on cardiac fibroblasts, we cannot exclude the possibility that other factors increase MFN-2, OPA-1 and PGC-1α levels in both cardiac fibroblasts or cardiomyocytes in the context of DCM. Further studies are needed to clarify the association between Prx-4 decrease and the increase in other mitochondrial proteins in DCM.

(致编辑的信)对:过氧化物还毒素-4在心力衰竭中的保护作用的回应。
我们感谢Ahmed等人对我们的研究“Galectin-3下调人心脏成纤维细胞中抗氧化过氧化物还蛋白-4”的来信[1]。Ahmed等人强调,扩张型心肌病(DCM)患者Prx-4水平降低[2],而MFN-2、OPA-1和PGC-1α水平升高[3]。此外,DCM中Gal-3的表达也增加[4]。在我们的研究中,我们在体外证明了Gal-3可以降低Prx-4,而不改变人心脏成纤维细胞中MFN-2或PGC-1α的水平。虽然心脏Prx-4的降低可能是Gal-3对心脏成纤维细胞作用的直接后果,但我们不能排除其他因素增加DCM背景下心脏成纤维细胞或心肌细胞中MFN-2、OPA-1和PGC-1α水平的可能性。需要进一步的研究来阐明Prx-4的减少与DCM中其他线粒体蛋白的增加之间的关系。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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