Department of Anesthesiology and Perioperative Medicine, Oregon Health and Science University, Portland, OR, U.S.A.
Section of Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, U.S.A.
Clin Sci (Lond). 2021 Jan 15;135(1):105-108. doi: 10.1042/CS20201319.
Although the numbers of patients affected by cardiorenal syndrome keeps increasing, we lack a complete understanding of the molecular pathways involved in its development and progression. Nitric oxide synthase (NOS) may play a role in cardiorenal syndrome, particularly cardiorenal syndrome type 2 (CRS2). However, complexities and paradoxical clinical findings have limited translation. In the current Clinical Science, Giam et al. (Clinical Science (2020) 134, 2755-2769) highlight the role of a key NOS substrate transporter, the cationic amino acid transporter-1, in preserving renal function in CRS2. In this commentary, we introduce the cardiorenal syndrome and the putative role that nitric oxide (NO) may play in the development of this disease and discuss the exciting findings of Giam et al. (Clinical Science (2020) 134, 2755-2769) and their tantalizing translational implications.
尽管受心肾综合征影响的患者人数不断增加，但我们仍不完全了解其发生和发展的分子途径。一氧化氮合酶（NOS）可能在心肾综合征中发挥作用，特别是心肾综合征 2 型（CRS2）。然而，其复杂性和矛盾的临床发现限制了其转化。在本期临床科学中，Giam 等人（Clinical Science (2020) 134, 2755-2769）强调了关键的 NOS 底物转运蛋白——阳离子氨基酸转运蛋白 1（cationic amino acid transporter-1）在保护 CRS2 患者肾功能中的作用。在这篇评论中，我们介绍了心肾综合征以及一氧化氮（NO）在该疾病发展过程中可能发挥的作用，并讨论了 Giam 等人（Clinical Science (2020) 134, 2755-2769）的令人兴奋的发现及其诱人的转化意义。
