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Exploring the implications of blocking renin-angiotensin-aldosterone system and fibroblast growth factor 23 in early left ventricular hypertrophy without chronic kidney disease

Watanabe, Kentarou Fujii, Hideki Okamoto, Kohei Kono, Keiji Goto, Shunsuke Nishi, Shinichi 神戸大学

2023.12.19

概要

Background: Whether fibroblast growth factor 23 (FGF23) directly induces left ventricular hypertrophy (LVH) remains controversial. Recent studies showed an association between FGF23 and the renin-angiotensin-aldosterone system (RAAS). The aim of this study was to investigate changes in FGF23 levels and RAAS parameters and their influences on LVH. Methods: In the first experiment, male C57BL/6J mice were divided into sham and transverse aortic constriction (TAC) groups. The TAC group underwent TAC at 8 weeks of age. At 1, 2, 3, and 4 weeks after TAC, the mice were sacrificed, and blood and urine samples were obtained. Cardiac expressions of FGF23 and RAAS-related factors were evaluated, and cardiac histological analyses were performed. In the second experiment, the sham and TAC groups were treated with vehicle, angiotensin-converting enzyme (ACE) inhibitor, or FGF receptor 4 (FGFR4) inhibitor and then evaluated in the same way as in the first experiment. Results: In the early stage of LVH without chronic kidney disease, serum FGF23 levels did not change but cardiac FGF23 expression significantly increased along with LVH progression. Moreover, serum aldosterone and cardiac ACE levels were significantly elevated, and cardiac ACE2 levels were significantly decreased. ACE inhibitor did not change serum FGF23 levels but significantly decreased cardiac FGF23 levels with improvements in LVH and RAAS-related factors, while FGFR4 inhibitor did not change the values. Conclusions: Not serum FGF23 but cardiac FGF23 levels and RAAS parameters significantly changed in the early stage of LVH without chronic kidney disease. RAAS blockade might be more crucial than FGF23 blockade for preventing LVH progression in this condition.

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system in cardiac myocytes and promotes the pro-fibrotic crosstalk between cardiac

myocytes and fibroblasts. Nephrol Dial Transplant (2018) 33(10):1722–34. doi:

10.1093/ndt/gfy006

1. Parfrey PS, Foley RN. The clinical epidemiology of cardiac disease in chronic renal

failure. J Am Soc Nephrol (1999) 10:1606–15. doi: 10.1681/ASN.V1071606

2. Foley RN, Parfrey PS, Harnett JD, Kent GM, Martin CJ, Murray DC, et al. Clinical

and echocardiographic disease in patients starting end-stage renal disease therapy.

Kidney Int (1995) 47:186–92. doi: 10.1038/ki.1995.22

25. Liu T, Wen H, Li H, Xu H, Xiao N, Liu R, et al. Oleic acid attenuates ang II

(Angiotensin II)-induced cardiac remodeling by inhibiting FGF23 (Fibroblast growth

factor 23) expression in mice. Hypertension (2020) 75(3):680–92. doi: 10.1161/

HYPERTENSIONAHA.119.14167

3. London GM, Pannier B, Guerin AP, Blacher J, Marchais SJ, Darne B, et al.

Alterations of left ventricular hypertrophy in and survival of patients receiving

hemodialysis: follow-up of an interventional study. J Am Soc Nephrol (2001)

12:2759–67. doi: 10.1681/ASN.V12122759

26. Okamoto K, Fujii H, Watanabe K, Goto S, Kono K, Nishi S. Changes of FGF23

and the renin-angiotensin-system in male mouse models of chronic kidney disease and

cardiac hypertrophy. J Endocr Soc (2021) 6(2):bvab187. doi: 10.1210/jendso/bvab187

4. Di Lullo L, Gorini A, Russo D, Santoboni A, Ronco C. Left ventricular

hypertrophy in chronic kidney disease patients: from pathophysiology to treatment.

Cardiorenal Med (2015) 5:254–66. doi: 10.1159/000435838

5. Wang X, Shapiro JI. Evolving concepts in the pathogenesis of uraemic

cardiomyopathy. Nat Rev Nephrol (2019) 15:159–75. doi: 10.1038/s41581-018-0101-8

27. Yang KK, Sui Y, Zhou HR, Shen J, Tan N, Huang YM, et al. Cross-talk between

AMP-activated protein kinase and renin-angiotensin system in uninephrectomised

rats. J Renin Angiotensin Aldosterone Syst (2016) 17(4):1470320316673231. doi:

10.1177/1470320316673231

6. Bao JF, Hu PP, She QY, Li A. A land of controversy: fibroblast growth factor-23

and uremic cardiac hypertrophy. J Am Soc Nephrol (2020) 31(7):1423–34. doi: 10.1681/

ASN.2020010081

28. Glosse P, Feger M, Mutig K, Chen H, Hirche F, Hasan AA, et al. AMP-activated

kinase is a regulator of fibroblast growth factor 23 production. Kidney Int (2018) 94

(3):491–501. doi: 10.1016/j.kint.2018.03.006

7. Faul C. FGF23 effects on the heart-levels, time, source, and context matter. Kidney

Int (2018) 94(1):7–11. doi: 10.1016/j.kint.2018.03.024

29. Böckmann I, Lischka J, Richter B, Deppe J, Rahn A, Fischer DC, et al. FGF23mediated activation of local RAAS promotes cardiac hypertrophy and fibrosis. Int J Mol

Sci (2019) 20(18):4634. doi: 10.3390/ijms20184634

8. Hsu HJ, Wu MS. Fibroblast growth factor 23: a possible cause of left ventricular

hypertrophy in hemodialysis patients. Am J Med Sci (2009) 337(2):116–22. doi:

10.1097/MAJ.0b013e3181815498

30. Mhatre KN, Wakula P, Klein O, Bisping E, Völkl J, Pieske B, et al. Crosstalk

between FGF23- and angiotensin II-mediated Ca 2+ signaling in pathological cardiac

hypertrophy. Cell Mol Life Sci (2018) 75(23):4403–16. doi: 10.1007/s00018-018-2885-x

9. Gutié rrez OM, Januzzi JL, Isakova T, Laliberte K, Smith K, Collerone G, et al.

Fibroblast growth factor 23 and left ventricular hypertrophy in chronic kidney disease.

Circulation (2009) 119(19):2545–52. doi: 10.1161/CIRCULATIONAHA.108.844506

31. Dai B, David V, Martin A, Huang J, Li H, Jiao Y, et al. Analysis identifying

FGF23 regulated genes in the kidney of a mouse CKD model. PloS One (2012) 7(9):

e44161. doi: 10.1371/journal.pone.0044161

10. Kirkpantur A, Balci M, Gurbuz OA, Afsar B, Canbakan B, Akdemir R, et al.

Serum fibroblast growth factor-23 (FGF-23) levels are independently associated with

left ventricular mass and myocardial performance index in maintenance haemodialysis

patients. Nephrol Dial Transplant (2011) 26(4):1346–54. doi: 10.1093/ndt/gfq539

32. Leifheit-Nestler M, Große Siemer R, Flasbart K, Richter B, Kirchhoff F, Ziegler

WH, et al. Induction of cardiac FGF23/FGFR4 expression is associated with left

ventricular hypertrophy in patients with chronic kidney disease. Nephrol Dial

Transplant (2016) 31(7):1088–99. doi: 10.1093/ndt/gfv421

11. Faul C, Amaral AP, Oskouei B, Hu MC, Sloan A, Isakova T, et al. FGF23 induces

left ventricular hypertrophy. J Clin Invest (2011) 121(11):4393–408. doi: 10.1172/

JCI46122

33. Takashi Y, Kinoshita Y, Hori M, Ito N, Taguchi M, Fukumoto S. Patients with

FGF23-related hypophosphatemic rickets/osteomalacia do not present with left

ventricular hypertrophy. Endocr Res (2017) 42(2):132–7. doi: 10.1080/

07435800.2016.1242604

12. Grabner A, Amaral AP, Schramm K, Singh S, Sloan A, Yanucil C, et al.

Activation of cardiac fibroblast growth factor receptor 4 causes left ventricular

hypertrophy. Cell Metab (2015) 22(6):1020–32. doi: 10.1016/j.cmet.2015.09.002

34. Herná ndez-Frı́as O, Gil-Peña H, Pé rez-Roldá n JM, Gonzá lez-Sanchez S, Ariceta

G, Chocró n S, et al. Risk of cardiovascular involvement in pediatric patients with Xlinked hypophosphatemia. Pediatr Nephrol (2019) 34(6):1077–86. doi: 10.1007/s00467018-4180-3

13. Unsal A, Budak SK, Koc Y, Basturk T, Sakaci T, Ahbap E, et al. Relationship of

fibroblast growth factor 23 with left ventricle mass index and coronary calcification in

chronic renal disease. Kidney Blood Press Res (2012) 36(1):55–64. doi: 10.1159/

000339026

35. Pastor-Arroyo EM, Gehring N, Krudewig C, Costantino S, Bettoni C, Knöpfel T,

et al. The elevation of circulating fibroblast growth factor 23 without kidney disease

does not increase cardiovascular disease risk. Kidney Int (2018) 94(1):49–59. doi:

10.1016/j.kint.2018.02.017

14. Shalhoub V, Shatzen EM, Ward SC, Davis J, Stevens J, Bi V, et al. FGF23

neutralization improves chronic kidney disease-associated hyperparathyroidism yet

increases mortality. J Clin Invest (2012) 122(7):2543–53. doi: 10.1172/JCI61405

36. Slavic S, Ford K, Modert M, Becirovic A, Handschuh S, Baierl A, et al. Genetic

ablation of Fgf23 or Klotho does not modulate experimental heart hypertrophy induced

by pressure overload. Sci Rep (2017) 7(1):11298. doi: 10.1038/s41598-017-10140-4

15. Liu ES, Thoonen R, Petit E, Yu B, Buys ES, Scherrer-Crosbie M, et al. Increased

circulating FGF23 does not lead to cardiac hypertrophy in the male hyp mouse model

of XLH. Endocrinology (2018) 159(5):2165–72. doi: 10.1210/en.2018-00174

37. Clinkenbeard EL, Megan L Noonan ML, Joseph C Thomas JC, Pu Ni P, Julia M

Hum JM, Mohammad Aref M, et al. Increased FGF23 protects against detrimental

cardio-renal consequences during elevated blood phosphate in CKD. JCI Insight (2019)

4(4):e123817. doi: 10.1172/jci.insight.123817

16. Stöhr R, Schuh A, Heine GH, Brandenburg V. FGF23 in cardiovascular disease:

innocent bystander or active mediator? Front Endocrinol (Lausanne) (2018) 9:351. doi:

10.3389/fendo.2018.00351

17. Leifheit-Nestler M, Haffner D. Paracrine effects of FGF23 on the heart. Front

Endocrinol (Lausanne) (2018) 9:278. doi: 10.3389/fendo.2018.00278

38. Maizel J, Six I, Dupont S, Secq E, Dehedin B, Barreto FC, et al. Effects of

sevelamer treatment on cardiovascular abnormalities in mice with chronic renal failure.

Kidney Int (2013) 84(3):491–500. doi: 10.1038/ki.2013.110

18. Knowles JW, Reddick RL, Jennette JC, Shesely EG, Smithies O, Maeda N.

Enhanced atherosclerosis and kidney dysfunction in eNOS(-/-)Apoe(-/-) mice are

ameliorated by enalapril treatment. J Clin Invest (2000) 105(4):451–8. doi: 10.1172/

JCI8376

39. Hao H, Xixian Li X, Li Q, Lin H, Chen Z, Xie J, et al. FGF23 promotes myocardial

fibrosis in mice through activation of b-catenin. Oncotarget (2016) 7(40):64649–64. doi:

10.18632/oncotarget.11623

19. Habashi JP, Doyle JJ, Holm TM, Aziz H, Schoenhoff F, Bedja D, et al.

Angiotensin II type 2 receptor signaling attenuates aortic aneurysm in mice through

ERK antagonism. Science (2011) 332(6027):361–5. doi: 10.1126/science.1192152

40. Matsui I, Oka T, Kusunoki Y, Mori D, Hashimoto N, Matsumoto A, et al.

Cardiac hypertrophy elevates serum levels of fibroblast growth factor 23. Kidney Int

(2018) 94(1):60–71. doi: 10.1016/j.kint.2018.02.018

20. Xin Z, Song X, Jiang B, Gongsun X, Song L, Qin Q, et al. Blocking FGFR4 exerts

distinct anti-tumorigenic effects in esophageal squamous cell carcinoma. Thorac

Cancer (2018) 9(12):1687–98. doi: 10.1111/1759-7714.12883

41. Schumacher D, Alampour-Rajabi S, Ponomariov V, Curaj A, Wu Z, Staudt M,

et al. Cardiac FGF23: new insights into the role and function of FGF23 after acute

myocardial infarction. Cardiovasc Pathol (2019) 40:47–54. doi: 10.1016/

j.carpath.2019.02.001

21. Joshi JJ, Coffey H, Corcoran E, Tsai J, Huang CL, Ichikawa K, et al. Share H3B6527 is a potent and selective inhibitor of FGFR4 in FGF19-driven hepatocellular

carcinoma. Cancer Res (2017) 77(24):6999–7013. doi: 10.1158/0008-5472.CAN-171865

42. Sadoshima J, Xu Y, Slayter HS, Izumo S. Autocrine release of angiotensin II

mediates stretch-induced hypertrophy of cardiac myocytes in vitro. Cell (1993) 75

(5):977–84. doi: 10.1016/0092-8674(93)90541-W

22. McGrath JC, Lilley E. Implementing guidelines on reporting research using

animals (ARRIVE etc.): new requirements for publication in BJP. Br J Pharmacol

(2015) 172(13):3189–93. doi: 10.1111/bph.12955

43. Rockman HA, Wachhorst SP, Mao L, Ross J Jr. ANG II receptor blockade

prevents ventricular hypertrophy and ANF gene expression with pressure overload in

mi c e . A m J Ph ys i ol ( 1 99 4 ) 26 6( 6 P t 2) : H2 46 8– 24 7 5. d o i: 10 . 11 52 /

ajpheart.1994.266.6.H2468

23. Zhang B, Umbach AT, Chen H, Yan J, Fakhri H, Fajol A, et al. Up-regulation of

FGF23 release by aldosterone. Biochem Biophys Res Commun (2016) 470(2):384–90.

doi: 10.1016/j.bbrc.2016.01.034

44. Czaya B, Seeherunvong W, Singh S, Yanucil C, Ruiz P, Quiroz Y, et al.

Cardioprotective effects of paricalcitol alone and in combination with FGF23

receptor inhibition in chronic renal failure: experimental and clinical studies. Am J

Hypertens (2019) 32(1):34–44. doi: 10.1093/ajh/hpy154

24. Leifheit-Nestler M, Kirchhoff F, Nespor J, Richter B, Soetje B, Klintschar M, et al.

Fibroblast growth factor 23 is induced by an activated renin-angiotensin-aldosterone

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