Cur@SF NPs exhibited a powerful effect in reducing the oxidative stress level and removing the accumulated iron in the myocardial tissue of FRDA mice. The behavioral and histological assays exhibited excellent therapeutic efficacy of Cur@SF NPs in improving neurological deficits and cardiomyopathy. Thus, we provide evidence for low-cost agent Cur@SF NPs by increasing their bioavailability, suggesting their potential in the treatment of FRDA disease.
Thursday, March 10, 2022
Cur@SF NPs alleviate Friedreich’s ataxia in a mouse model through synergistic iron chelation and antioxidation
Li Xu, Zichen Sun, Zhiyao Xing, Yutong Liu, Hongting Zhao, Zhongmin Tang, Yu Luo, Shuangying Hao & Kuanyu Li; J Nanobiotechnol 20, 118 (2022). doi;10.1186/s12951-022-01333-9
Should Advanced Friedreich’s Ataxia Be a Contraindication for Heart Transplantation? A Case Report of a Successful Procedure in a 58-Year-Old Patient
Valero, M.J.; Muñoz-Blanco, J.L.; Sanchez, A.G.; Cuerpo, G.; Castrodeza, J.; Navas, P.; Sousa, I.; Villa, A.; Fernández-Avilés, F.; Martínez-Sellés; J. Cardiovasc. Dev. Dis. 2022, 9, 80. doi:10.3390/jcdd9030080
We conclude that HT is a safe option for end-stage heart disease in selected patients with FA. A multidisciplinary team should assess utility, justice, quality of life, and life expectancy. Patient involvement in the decision is essential.
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