参考文献/References:
[1] Ronco C,McCullough P,Anker SD,et al. Cardio-renal syndromes:report from the consensus conference of the Acute Dialysis Quality Initiative[J]. Eur Heart J,2010,31(6):703-711.
[2] United States Renal Data System. 2020 USRDS Annual Data Report:Epidemiology of kidney disease in the United States (National Institutes of Health,National Institute of Diabetes and Digestive and Kidney Diseases,2020) [EB/OL]. Bethesda:MD,(2020)[2024-04-21]. https://usrds-adr.niddk.nih.gov/.
[3] Lim YJ,Sidor NA,Tonial NC,et al. Uremic toxins in the progression of chronic kidney disease and cardiovascular disease:mechanisms and therapeutic targets[J]. Toxins (Basel),2021,13(2):142.
[4] Rysz J,Franczyk B,?awiński J,et al. The impact of CKD on uremic toxins and gut microbiota[J]. Toxins (Basel),2021,13(4):252.
[5] He M,Wei W,Zhang Y,et al. Gut microbial metabolites SCFAs and chronic kidney disease[J]. J Transl Med,2024,22:172.
[6] Yamaguchi K,Yisireyili M,Goto S,et al. Indoxyl sulfate activates NLRP3 inflammasome to induce cardiac contractile dysfunction accompanied by myocardial fibrosis and hypertrophy[J]. Cardiovasc Toxicol,2022,22(4):365-377.
[7] Savira F,Kompa AR,Magaye R,et al. Apoptosis signal-regulating kinase 1 inhibition reverses deleterious indoxyl sulfate-mediated endothelial effects[J]. Life Sci,2021,272:119267.
[8] Yamagami F,Tajiri K,Yumino D,et al. Uremic toxins and atrial fibrillation:mechanisms and therapeutic implications[J]. Toxins (Basel),2019,11(10):597.
[9] van Ham WB,Cornelissen CM,Polyakova E,et al. Pro-arrhythmic potential of accumulated uremic toxins is mediated via vulnerability of action potential repolarization[J]. Int J Mol Sci,2023,24(6):5373.
[10] Karpushev AV,Mikhailova VB,Klimenko ES,et al. SGLT2 inhibitor Empagliflozin modulates ion channels in adult zebrafish heart[J]. Int J Mol Sci,2022,23(17):9559.
[11] Tang WHW,Wang Z,Levison BS,et al. Intestinal microbial metabolism of phosphatidylcholine and cardiovascular risk[J]. N Engl J Med,2013,368(17):1575-1584.
[12] Zhang Y,Wang Y,Ke B,et al. TMAO:how gut microbiota contributes to heart failure[J]. Transl Res,2021,228:109-125.
[13] Wu K,Yuan Y,Yu H,et al. The gut microbial metabolite trimethylamine N-oxide aggravates GVHD by inducing M1 macrophage polarization in mice[J]. Blood,2020,136(4):501-515.
[14] Shi W,Huang Y,Yang Z,et al. Reduction of TMAO level enhances the stability of carotid atherosclerotic plaque through promoting macrophage M2 polarization and efferocytosis[J]. Biosci Rep,2021,41(6):BSR20204250.
[15] Wang Z,Roberts AB,Buffa JA,et al. Non-lethal inhibition of gut microbial trimethylamine production for the treatment of atherosclerosis[J]. Cell,2015,163(7):1585-1595.
[16] Xu J,Moore BN,Pluznick JL. Short-chain fatty acid receptors and blood pressure regulation:Council on Hypertension Mid-Career Award for Research Excellence 2021[J]. Hypertension,2022,79(10):2127-2137.
[17] Pluznick JL,Protzko RJ,Gevorgyan H,et al. Olfactory receptor responding to gut microbiota-derived signals plays a role in renin secretion and blood pressure regulation[J]. Proc Natl Acad Sci U S A,2013,110(11):4410-4415.
[18] Datta S,Pasham S,Inavolu S,et al. Role of gut microbial metabolites in cardiovascular diseases—Current Insights and the road ahead[J]. Int J Mol Sci,2024,25(18):10208.
[19] Smith PM,Howitt MR,Panikov N,et al. The microbial metabolites,short-chain fatty acids,regulate colonic treg cell homeostasis[J]. Science,2013,341(6145):569-573.
[20] Yan J,Pan Y,Shao W,et al. Beneficial effect of the short-chain fatty acid propionate on vascular calcification through intestinal microbiota remodelling[J]. Microbiome,2022,10(1):195.
[21] Zeder K,Siew ED,Kovacs G,et al. Pulmonary hypertension and chronic kidney disease:prevalence,pathophysiology and outcomes[J]. Nat Rev Nephrol,2024,20(11):742-754.
[22] Matsushita K,Ballew SH,Wang AYM,et al. Epidemiology and risk of cardiovascular disease in populations with chronic kidney disease[J]. Nat Rev Nephrol,2022,18(11):696-707.
[23] di Lullo L,Reeves PB,Bellasi A,et al. Cardiorenal syndrome in acute kidney injury[J]. Semin Nephrol,2019,39(1):31-40.
[24] van den Eynde J,Jacquemyn X,Cloet N,et al. Arteriovenous fistulae in chronic kidney disease and the heart:physiological,histological,and transcriptomic characterization of a novel rat model[J]. J Am Heart Assoc,2022,11(20):e027593.
[25] Cozzolino M,Ciceri P,Galassi A,et al. The key role of phosphate on vascular calcification[J]. Toxins (Basel),2019,11(4):213.
[26] Carrillo-López N,Martínez-Arias L,Alonso-Montes C,et al. The receptor activator of nuclear factor κΒ ligand?receptor leucine-rich repeat-containing G-protein-coupled receptor 4?contributes to parathyroid hormone-induced vascular calcification[J]. Nephrol Dial Transplant,2021,36(4):618-631.
[27] Arase H,Yamada S,Tanaka S,et al. Association between plasma intact parathyroid hormone levels and the prevalence of atrial fibrillation in patients with chronic kidney disease—The Fukuoka Kidney Disease Registry Study[J]. Circ J,2020,84(7):1105-1111.
[28] Trevisan C,Rossi A,Curreri C. Increased parathyroid hormone concentration as a biomarker of atrial fibrillation in severe aortic stenosis:Editorial comment[J]. Kardiol Pol,2024,82(11):1055-1056.
[29] Han X,Cai C,Xiao Z,et al. FGF23 induced left ventricular hypertrophy mediated by FGFR4 signaling in the myocardium is attenuated by soluble Klotho in mice[J]. J Mol Cell Cardiol,2020,138:66-74.
[30] Ishigami J,Grams ME,Naik RP,et al. Hemoglobin,albuminuria,and kidney function in cardiovascular risk:the ARIC (Atherosclerosis Risk in Communities) Study[J]. J Am Heart Assoc,2018,7(2):e007209.
[31] Packer M. Mutual antagonism of hypoxia-inducible factor isoforms in cardiac,vascular,and renal disorders[J]. JACC Basic Transl Sci,2020,5(9):961-968.
[32] Zhao Y,Xiong W,Li C,et al. Hypoxia-induced signaling in the cardiovascular system:pathogenesis and therapeutic targets[J]. Signal Transduct Target Ther,2023,8(1):431.
[33] Buliga-Finis ON,Ouatu A,Tanase DM,et al. Managing Anemia:point of convergence for heart failure and chronic kidney disease?[J]. Life (Basel),2023,13(6):1311.
[34] Dobre MA,Ahlawat S,Schelling JR. Chronic kidney disease associated cardiomyopathy:recent advances and future perspectives[J]. Curr Opin Nephrol Hypertens,2024,33(2):203-211.
[35] Amann K,Ritz E. The heart in renal failure:morphological changes of the myocardium—New insights[J]. J Clin Basic Cardiol,2001,4:109-113.
[36] van Ham WB,Cornelissen CM,van Veen TAB. Uremic toxins in chronic kidney disease highlight a fundamental gap in understanding their detrimental effects on cardiac electrophysiology and arrhythmogenesis[J]. Acta Physiol (Oxf),2022,236(3):e13888.
[37] Munguia-Galaviz FJ,Gutierrez-Mercado YK,Miranda-Diaz AG,et al. Cardiac transcriptomic changes induced by early CKD in mice reveal novel pathways involved in the pathogenesis of Cardiorenal syndrome type 4[J]. Heliyon,2024,10(6):e27468.
[38] Chade AR,Eirin A. Cardiac micro-RNA and transcriptomic profile of a novel swine model of chronic kidney disease and left ventricular diastolic dysfunction[J]. Am J Physiol Heart Circ Physiol,2022,323(4):H659-H669.
[39] Yu F,Peng Z,Gao N,et al. Sinomenine attenuates uremia vascular calcification by miR-143-5p[J]. Sci Rep,2025,15(1):1798.
[40] Di J,Yang M,Zhou H,et al. MicroRNA-21-containing microvesicles from tubular epithelial cells promote cardiomyocyte hypertrophy[J]. Ren Fail,2021,43(1):391-400.