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(Letter to the Editor) Response to: protective role of peroxiredoxin-4 in heart failure
1Cardiovascular Translational Research, NavarraBiomed (Miguel Servet Foundation) Irunlarrea 3, 31008 Pamplona, Spain.
Insights
Galectin-3 (Gal-3) reduces antioxidant peroxiredoxin-4 (Prx-4) in human cardiac cells. This finding may explain Prx-4 decrease in dilated cardiomyopathy, though other factors also influence mitochondrial proteins.
Area of Science:
- Cardiovascular Biology
- Mitochondrial Function
- Oxidative Stress
Background:
- Dilated cardiomyopathy (DCM) is associated with decreased peroxiredoxin-4 (Prx-4) and increased mitochondrial proteins like MFN-2, OPA-1, and PGC-1α.
- Galectin-3 (Gal-3) expression is also elevated in DCM patients.
- The precise relationship between Gal-3, Prx-4, and other mitochondrial proteins in DCM remains unclear.
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.
