Novel Insights into the Cardioprotective Effects of Calcitriol in Myocardial Infarction

Yang, Simin; Wang, Chunmiao; Ruan, Cheng-shao; Chen, Mei‐Ling; Cao, Ran; Sheng, Liang; Chang, Naiying; Xu, Tong; Zhao, Peiwen; Liu, Xuesheng; Zhu, Feng-qin; Xiao, Qingzhong; Gao, Shan

doi:10.3390/cells11101676

Cited by 8 publications

(8 citation statements)

References 40 publications

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“…Non-invasive tests of cardiac function were performed before the mice sacrificed. Cardiac function indicators such as left ventricular ejection fraction (LVEF), fractional shortening (LVFS), and internal diameter end diastole (LVIDd) and end systole (LVIDs) were collected using a Doppler ultrasound diagnostic instrument (VINNO 6vet) as previously reported ( Yang et al, 2022 ).…”

Section: Methodsmentioning

confidence: 99%

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Xin-Ji-Er-Kang protects heart from ischemia-reperfusion injury by rebalancing lipid metabolism

et al. 2022

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Background and Purpose: We have previously reported a cardioprotective effect with Xin-Ji-Er-Kang (XJEK) treatment in mice with myocardial infarction (MI)-induced heart failure, but no report about its potential functions in myocardial ischemia-reperfusion (MIR) injury. Here we studied the therapeutic effects of XJEK on MIR injury and investigated the mechanisms involved.Experimental Approach: MIR model of Balb/c mice induced by left anterior descending coronary artery ligation for half an hour, followed by reperfusion, was utilized to study the potential therapeutic effects of XJEK on MIR-induced cardiac injury. Ultra-performance liquid chromatography tandem Orbitrap mass spectrometry platform was used for studying serum lipid metabolic signatures.Key Results: MIR caused cardiac dysfunctions, cardiac injury, myocardial fibrosis, and increased inflammation, and all the observed abnormalities caused by MIR were largely corrected by XJEK treatment. Mechanistically, XJEK exerts its cardioprotective effect in the context of MIR injury by suppressing MIR-induced inflammation and dysregulation of serum lipid metabolism.Conclusion and Implications: We have demonstrated for the first time that XJEK protects heart from MIR injury by restoring dysregulated lipidomics. Our data provide new evidence to support a therapeutic effect for XIEK on MIR-induced cardiac injury, and pave the way for exploring the therapeutic potential of XJEK in large animal study and early clinical trial.

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Section: Methodsmentioning

confidence: 99%

“…Frontiers in Pharmacology frontiersin.org fractional shortening (LVFS), and internal diameter end diastole (LVIDd) and end systole (LVIDs) were collected using a Doppler ultrasound diagnostic instrument (VINNO 6vet) as previously reported (Yang et al, 2022).…”

Section: Echocardiographic Measurementsmentioning

confidence: 99%

Xin-Ji-Er-Kang protects heart from ischemia-reperfusion injury by rebalancing lipid metabolism

et al. 2022

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“…VDR overexpression significantly ameliorates myocardial fibrosis in pressure-overloaded hearts and decreases mRNA expression levels of collagen I ( Col1 ), collagen III ( Col3 ), and TIMP-1 [ 34 ]. Notably, 1,25(OH) 2 D 3 and calcitriol supplementation ameliorates myocardial fibrosis by enhancing VDR proteins [ 35 , 36 , 37 ]. The above studies suggest that VDR regulates ECM metabolism in cardiomyocytes, which plays a role in regulating myocardial fibrosis.…”

Section: Introductionmentioning

confidence: 99%

“…Subsequently, the complex is transported to the nucleus and then combined with the promoter region of the target gene to regulate gene expression [ 38 ]. VDR is a nuclear hormone receptor, which exists in most functional organs of the body, especially in the heart and blood vessels [ 37 , 39 ]. In the cardiovascular system, the deletion of VDR is associated with adverse cardiac remodeling, hypertrophy, and inflammatory response [ 34 , 40 ].…”

Section: Introductionmentioning

confidence: 99%

“…In the cardiovascular system, the deletion of VDR is associated with adverse cardiac remodeling, hypertrophy, and inflammatory response [ 34 , 40 ]. While the activation of VDR can improve cardiac dysfunction, it can also alleviate myocardial fibrosis and inflammatory responses [ 35 , 37 , 40 , 41 ]. These results suggest that VDR may be a potential target for the treatment of CVD.…”

Section: Introductionmentioning

confidence: 99%

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Aerobic Exercise Ameliorates Myocardial Fibrosis via Affecting Vitamin D Receptor and Transforming Growth Factor-β1 Signaling in Vitamin D-Deficient Mice

et al. 2023

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Myocardial fibrosis is a pathological phenomenon associated with cardiovascular disease (CVD) that plays a crucial role in the development of heart diseases. Vitamin D deficiency can promote the development of CVD and exercise plays a role in the treatment of CVD. This study aimed to explore the effects of 12-week aerobic exercise training on myocardial fibrosis in vitamin D-deficient mice. A vitamin D-deficient mouse model was induced by a vitamin D-deficient (0 IU Vitamin D3/kg) diet. Twenty-four C57BL/6J male mice were randomly divided into three groups: a control sedentary group (CONS, n = 8), a vitamin D-deficient sedentary group (VDDS, n = 8), and a vitamin D-deficient exercise group (VDDE, n = 8) which was aerobically trained for 12 weeks. The results showed that the serum 25-hydroxyvitamin D [25(OH)D] levels of the VDDS group were <50 nmol/L, which was significantly lower than that of the CONS group. Compared with the CONS group, the VDDS group showed cardiac dysfunction and significant fibrosis, together with lower vitamin D receptor (VDR) mRNA and protein expression levels, higher mRNA expression levels of profibrotic and inflammatory factors, and higher transforming growth factor-β1 (TGF-β1) and phospho-Smad2/3 (P-Smad2/3) protein expression levels. Serum 25(OH)D levels in the VDDE group were significantly higher than those in the VDDS group. Compared with the VDDS group, the VDDE group showed improved cardiac function and alleviated myocardial fibrosis. Meanwhile, the VDDE group had significantly higher VDR mRNA and protein expression levels; lower mRNA expression levels of profibrotic and inflammatory factors; and lower TGF-β1 and P-Smad2/3 protein expression levels. In conclusion, aerobic exercise training remains a promising intervention for treating myocardial fibrosis in vitamin D deficiency.

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Effect of exogenous calcitriol on myopia development and axial length in guinea pigs with form deprivation myopia

Liang,

Shi,

et al. 2024

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The annual increase in myopia prevalence poses a significant economic and health challenge. Our study investigated the effect of calcitriol role in myopia by inducing the condition in guinea pigs through form deprivation for four weeks. Untargeted metabolomics methods were used to analyze the differences in metabolites in the vitreous body, and the expression of vitamin D receptor (VDR) in the retina was detected. Following form deprivation, the guinea pigs received intraperitoneal injections of calcitriol at different concentrations. We assessed myopia progression using diopter measurements and biometric analysis after four weeks. Results indicated that form deprivation led to a pronounced shift towards myopia, characterized by reduced choroidal and scleral thickness, disorganized collagen fibers, and decreased scleral collagen fiber diameter. Notably, a reduction in calcitriol expression in vitreous body, diminished vitamin D and calcitriol levels in the blood, and decreased VDR protein expression in retinal tissues were observed in myopic guinea pigs. Calcitriol administration effectively slowed myopia progression, preserved choroidal and scleral thickness, and prevented the reduction of scleral collagen fiber diameter. Our findings highlight a significant decrease in calcitriol and VDR expressions in myopic guinea pigs and demonstrate that exogenous calcitriol supplementation can halt myopia development, enhancing choroidal and scleral thickness and scleral collagen fiber diameter.

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Novel Insights into the Cardioprotective Effects of Calcitriol in Myocardial Infarction

Cited by 8 publications

References 40 publications

Xin-Ji-Er-Kang protects heart from ischemia-reperfusion injury by rebalancing lipid metabolism

Xin-Ji-Er-Kang protects heart from ischemia-reperfusion injury by rebalancing lipid metabolism

Aerobic Exercise Ameliorates Myocardial Fibrosis via Affecting Vitamin D Receptor and Transforming Growth Factor-β1 Signaling in Vitamin D-Deficient Mice

Effect of exogenous calcitriol on myopia development and axial length in guinea pigs with form deprivation myopia

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