Iron is essential for all the lives on earth but may trigger a switch toward ferroptosis, a novel form of regulated necrosis. Carbonic anhydrases (CAs) are ubiquitous enzymes from microbes to humans. The primary function of CAs is to regulate cellular pH by hydrating carbon dioxide (CO₂) to protons (H⁺) and bicarbonate ions (HCO₃⁻). Furthermore, CAs play roles in biosynthetic reactions, such as gluconeogenesis, lipogenesis, ureagenesis and are also associated with tumor metabolism, suggesting that CAs may be a potential target for the treatment of cancers. We have recently revealed a novel function of CA IX in ferroptosis-resistance by using human malignant mesothelioma cells. Herein, we aim to review the potential molecular association between ferroptosis and CAs, from the viewpoint of iron-metabolism, lipogenesis and signaling pathways both under physiological and pathological contexts.

铁对于地球上的所有生命都是必不可少的，但它可能会触发向铁锈病的转变，铁屑病是一种新型的坏死性调节形式。碳酸酐酶（CAs）是从微生物到人类的普遍存在的酶。CA的主要功能是通过水合的二氧化碳（CO以调节细胞pH ₂）质子（H ⁺）和碳酸氢根离子（HCO ₃ ^-）。此外，CA在生物合成反应中发挥作用，例如糖异生，脂肪生成，尿素生成，并且还与肿瘤代谢相关，这表明CA可能是治疗癌症的潜在靶标。我们最近通过使用人类恶性间皮瘤细胞揭示了CA IX在抗铁锈病中的新功能。在本文中，我们旨在从生理和病理学背景下的铁代谢，脂肪生成和信号传导途径的角度，审查肥大症和CAs之间的潜在分子关联。