Modern medicine increasingly focuses on the treatment and alleviation of diseases before they make substantial progress, and organ fibrosis has always been an important stage in the occurrence of substantial pathological changes in organs. The important characteristics of organ fibrosis are the excessive proliferation of myofibroblasts and the excessive deposition of extracellular matrix, which are regulated by a variety of complex signaling pathways and cytokines. The process of fibrosis cannot be separated from the functional support of mitochondria. The process of energy production in mitochondria is inseparable from the electron transfer brought about by the transformation of ROS (Reactive oxygen species) among various forms. N6-methyladenosine (m6A) modification, one of the most abundant RNA methylation modifications, dynamically regulates RNA stability, splicing, and translation through methyltransferases (such as METTL3 and METTL14), demethylases (such as FTO and ALKBH5), and reader proteins (such as YTH family proteins), thereby playing a crucial role in gene expression regulation. Recent studies have demonstrated that m6A plays an indispensable role in organ fibrosis by modulating mitochondrial ROS production, thereby influencing the progression of fibrosis. This review summarizes the regulatory mechanisms of m6A-related enzymes in mitochondrial ROS during cardiac, hepatic, pulmonary, and renal fibrosis, highlighting the critical role of m6A modification in organ fibrosis. By affecting mitochondrial function and ROS levels, m6A modification regulates cell proliferation, apoptosis, and differentiation in fibrotic processes, thereby playing a key role in the initiation and progression of organ fibrosis. Furthermore, we discuss potential therapeutic strategies targeting m6A modification and mitochondrial ROS.