RNA modifications in organ fibrosis: bibliometric evolution, convergent mechanisms, and emerging pharmacological targets.

Fibrosis is a common pathological outcome of chronic tissue injury, yet effective antifibrotic pharmacotherapies remain scarce. RNA modifications are covalent chemical alterations of the ribose sugar or nitrogenous bases of RNA without changing the RNA sequence. This study aimed to map the evolution of research linking RNA modifications to fibrosis and to integrate the bibliometric signals with mechanistic and pharmacological evidence. We searched the Web of Science Core Collection on June 3, 2026. After restriction to English-language articles and reviews and exclusion of two retracted publications, 739 records were analyzed using VOSviewer, followed by a mechanism-oriented narrative synthesis. The dataset comprised 634 articles and 105 reviews, accumulated 16,558 citations (22.41 citations per record; mean annual citation rate, 4.45), and reached an h-index of 60. Annual publication output remained limited for many years but accelerated after 2021 and peaked at 177 records in 2025. China and the USA were the principal contributors. Renal, cardiac, hepatic, and pulmonary fibrosis were the major organ-specific domains. N6-methyladenosine (m6A) dominated the literature, whereas 5-methylcytosine, adenosine-to-inosine editing, pseudouridine, N4-acetylcytidine, N7-methylguanosine, and N1-methyladenosine represented emerging themes. Keyword and citation analyses indicated a shift from descriptive studies of RNA methylation toward enzyme-specific and mechanism-driven research involving METTL3, FTO, ALKBH5, oxidative stress, ferroptosis, extracellular matrix remodeling, and non-coding RNA crosstalk. Evidence indicates that RNA modification writers, erasers, and readers converge on TGF-β/Smad, PI3K/Akt, and Wnt/β-catenin signaling, as well as inflammation, oxidative stress, regulated cell death, fibroblast activation, mesenchymal transition, and extracellular matrix deposition. Research on RNA modifications in fibrosis has expanded rapidly and is moving toward pharmacological exploration. However, candidate regulators remain preclinical targets whose therapeutic value depends on selectivity, cell-specific delivery, target-engagement assays, and validation in human diseases.