Maxacalcitol (22-Oxacalcitriol (OCT)) Retards Progression of Left Ventricular Hypertrophy with Renal Dysfunction Through Inhibition of Calcineurin-NFAT Activity.

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Tytuł:: Maxacalcitol (22-Oxacalcitriol (OCT)) Retards Progression of Left Ventricular Hypertrophy with Renal Dysfunction Through Inhibition of Calcineurin-NFAT Activity.
Autorzy:: Inoue K; Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
Matsui I; Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan. .
Hamano T; Department of Inter-Organ Communication Research in Kidney Disease, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.; Department of Nephrology, Nagoya City University Graduate School of Medical Science and Medical School, 1 Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Aichi, 467-8601, Japan.
Okuda K; Cardiovascular Division, Osaka Saiseikai Senri Hospital, Suita, Osaka, 565-0862, Japan.
Tsukamoto Y; Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
Matsumoto A; Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
Shimada K; Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
Yasuda S; Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
Katsuma Y; Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
Takabatake Y; Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
Tanaka M; Department of Nephrology, Tanaka Kitanoda Hospital, 707 Kitanoda, Sakai-ku, Sakai, Osaka, 599-8123, Japan.
Tanaka N; Department of Nephrology, Tanaka Kitanoda Hospital, 707 Kitanoda, Sakai-ku, Sakai, Osaka, 599-8123, Japan.
Mano T; Department of Cardiology, Kansai Rosai Hospital, 3-1-69 Inabasou, Amagasaki, Hyogo, 660-8511, Japan.
Minamino T; Department of Cardiorenal and Cerebrovascular Medicine, Kagawa University Graduate School of Medicine, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa, 761-0793, Japan.
Sakata Y; Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
Isaka Y; Department of Nephrology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka, 565-0871, Japan.
Źródło:: Cardiovascular drugs and therapy [Cardiovasc Drugs Ther] 2021 Apr; Vol. 35 (2), pp. 381-397. Date of Electronic Publication: 2020 Nov 18.
Typ publikacji:: Clinical Trial; Journal Article
Język:: English
Imprint Name(s):: Publication: Norwell Ma : Kluwer Academic For The International Society For Cardiovascular Pharmacotherapy
Original Publication: [Norwell, MA] : Martinus Nijhoff Pub., [c1987-
MeSH Terms:: Calcitriol/*analogs & derivatives
Hypertrophy, Left Ventricular/*drug therapy
Hypertrophy, Left Ventricular/*etiology
Hypertrophy, Left Ventricular/*pathology
Renal Insufficiency/*complications
Aged ; Animals ; Calcineurin/drug effects ; Calcitriol/pharmacology ; Cell Culture Techniques ; Disease Models, Animal ; Female ; Humans ; Male ; Middle Aged ; Myocytes, Cardiac/drug effects ; NFATC Transcription Factors/metabolism ; Pregnancy ; Rats ; Rats, Wistar ; Retrospective Studies
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Contributed Indexing:: Keywords: Active vitamin D analog; Angiotensin II; Atrogin1; Calcineurin A; Chronic kidney disease; Left ventricular hypertrophy
Substance Nomenclature:: 0 (NFATC Transcription Factors)
EC 3.1.3.16 (Calcineurin)
FXC9231JVH (Calcitriol)
N2UJM5NBF6 (maxacalcitol)
Entry Date(s):: Date Created: 20201118 Date Completed: 20211213 Latest Revision: 20211214
Update Code:: 20240105
DOI:: 10.1007/s10557-020-07111-9
PMID:: 33206298
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Purpose: Left ventricular hypertrophy (LVH) is a cardiovascular complication highly prevalent in patients with chronic kidney disease (CKD). Previous studies analyzing 1α-hydroxylase or vitamin D receptor (Vdr) knockout mice revealed active vitamin D as a promising agent inhibiting LVH progression. Paricalcitol, an active vitamin D analog, failed to suppress the progression of LV mass index (LVMI) in pre-dialysis patients with CKD. As target genes of activated VDR differ depending on its agonists, we examined the effects of maxacalcitol (22-oxacalcitriol: OCT), a less calcemic active vitamin D analog, on LVH in hemodialysis patients and animal LVH models with renal insufficiency.
Methods: In retrospective cohort study, patients treated with OCT who underwent hemodialysis were enrolled. Using cardiac echocardiography, LV mass was evaluated by the area-length method. In animal study, angiotensin II (Ang II)-infused Wister rats with heminephrectomy or Ang II-stimulated neonatal rat ventricular myocytes (NRVM) were treated with OCT.
Results: OCT significantly inhibited the progression of LVMI in hemodialysis patients. In Ang II-infused heminephrectomized rats, OCT suppressed the progression of LVH in a blood pressure-independent manner. OCT also suppressed the activity of calcineurin in the left ventricle of model rats. Specifically, OCT reduced the protein levels of calcineurin A, but not the mRNA levels of Ppp3ca (calcineurin Aα). Luciferase assays showed that OCT increased the promoter activity of Fbxo32 (atrogin1), an E3 ubiquitin ligase targeting calcineurin A. Finally, OCT promoted ubiquitination and degradation of calcineurin A.
Conclusion: Our works indicated that OCT retards progression of LVH through calcineurin-NFAT pathway, which reveal a novel aspect of OCT in attenuating pathological LVH.

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