Mariana Rosca

(�/�X��:pc�F0g6m��@MFD���MC%����ze�W�1d[J"��>\�1�Z��ό1���ܿ�7��^�m.|�*�CK�O � w S�8<俿����'�T��� ��pp��Ab��% ��ߕ��+8d���$�>T:��I���L�T ����Qw�<����\�u�6=����Q'��8�L�D � d����%�K/K�~ e���+D�]�*� ���/��g"T�*�3(6fu�$��4^�t~�z���ׅ���b�3F���&|�_��om�k%6c�q��� �]ۊY���1��� �PgkQ��:��H�����*��TQ�_�K��FF��Ɂ$�a�6�d��������� YEΆ`����N�S%U��Rh��r"i>ԙT��CMiR�4�?�O&�9�C=��8��7a.���P7]K�l�v�� R�����_�*[#�{C�?Bf�� zHJOT'5�����%�@�T�zb(�l9�X���V�nU�^_I�.����dL�h~� zDە�~=�5�-}��GxD�k��~�2Lv�������P�v_�k�єМ...

Introduction Diabetic retinopathy remains the leading cause of vision loss in the working age adults, and the exact molecular mechanism of this devastating disease remains unclear. Constant chronic exposure to high circulating glucose damages mitochondria and increased production of mitochondrial free radicals affects major metabolic abnormalities associated with the development of diabetic retinopathy (1–3).