Effect of vitamin D on cardiac hypertrophy in D-galactose-induced aging model through cardiac mitophagy.


Journal

Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234

Informations de publication

Date de publication:
Dec 2023
Historique:
received: 29 08 2023
accepted: 02 10 2023
medline: 27 11 2023
pubmed: 3 11 2023
entrez: 3 11 2023
Statut: ppublish

Résumé

Cardiac apoptosis plays a key role in increased morbidity associated with aging-induced-cardiac disorder. Mitochondria play an important role in cardiac apoptosis, and dynamin-related protein 1 (Drp1), as a main mediator of mitochondrial fission, can trigger the mitophagy process to sustain the mitochondrial quality. The present study was done to determine the effect of vitamin D (VitD) treatment on cardiac hypertrophy through mitophagy regulation in aged animals induced by D-galactose (D-GAL). Male Wistar rats were randomly divided into four groups: control, D-GAL (aging group), D-GAL co-injected with VitD (D-GAL ± VitD), and D-GAL plus ethanol (D-GAL ± Ethanol). Aging was induced by an intraperitoneal (i.p.) administration of D-GAL at 150 mg/kg daily for eight weeks and also VitD (400 IU/kg) or ethanol was injected (i.p.) into aging rats. Then, the levels of cardiac mitophagy and cardiac apoptosis were determined by measuring the expression of tensin homologue (PTEN)-induced putative kinase 1 (PINK1), Drp1, Bcl2-Associated X (Bax), and B-cell lymphoma 2 (Bcl2) genes. Aging in rats was associated with a reduction in mitophagy and also an increase in apoptosis of the heart through down-regulation of Drp1, PINK1, and Bcl2 genes and also up-regulation of Bax. However, VitD improved cardiac hypertrophy through cardiac mitophagy in D-GAL-induced aging rats. VitD can inhibit cardiac hypertrophy by an increase in mitophagy and a decrease in apoptosis in the aging heart. The illustration of the suggested mechanism underlying of Vitamin D in cardiac hypertrophy induced by aging.

Sections du résumé

BACKGROUND BACKGROUND
Cardiac apoptosis plays a key role in increased morbidity associated with aging-induced-cardiac disorder. Mitochondria play an important role in cardiac apoptosis, and dynamin-related protein 1 (Drp1), as a main mediator of mitochondrial fission, can trigger the mitophagy process to sustain the mitochondrial quality. The present study was done to determine the effect of vitamin D (VitD) treatment on cardiac hypertrophy through mitophagy regulation in aged animals induced by D-galactose (D-GAL).
METHODS AND RESULTS RESULTS
Male Wistar rats were randomly divided into four groups: control, D-GAL (aging group), D-GAL co-injected with VitD (D-GAL ± VitD), and D-GAL plus ethanol (D-GAL ± Ethanol). Aging was induced by an intraperitoneal (i.p.) administration of D-GAL at 150 mg/kg daily for eight weeks and also VitD (400 IU/kg) or ethanol was injected (i.p.) into aging rats. Then, the levels of cardiac mitophagy and cardiac apoptosis were determined by measuring the expression of tensin homologue (PTEN)-induced putative kinase 1 (PINK1), Drp1, Bcl2-Associated X (Bax), and B-cell lymphoma 2 (Bcl2) genes. Aging in rats was associated with a reduction in mitophagy and also an increase in apoptosis of the heart through down-regulation of Drp1, PINK1, and Bcl2 genes and also up-regulation of Bax. However, VitD improved cardiac hypertrophy through cardiac mitophagy in D-GAL-induced aging rats.
CONCLUSION CONCLUSIONS
VitD can inhibit cardiac hypertrophy by an increase in mitophagy and a decrease in apoptosis in the aging heart. The illustration of the suggested mechanism underlying of Vitamin D in cardiac hypertrophy induced by aging.

Identifiants

pubmed: 37921981
doi: 10.1007/s11033-023-08875-7
pii: 10.1007/s11033-023-08875-7
doi:

Substances chimiques

Vitamin D 1406-16-2
Galactose X2RN3Q8DNE
bcl-2-Associated X Protein 0
Vitamins 0
Protein Kinases EC 2.7.-
Ethanol 3K9958V90M

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

10147-10155

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Nature B.V.

Références

Tepp K et al (2016) Bioenergetics of the aging heart and skeletal muscles: modern concepts and controversies. Ageing Res Rev 28:1–14
pubmed: 27063513
Chadda KR et al (2018) Ageing, the autonomic nervous system and arrhythmia: from brain to heart. Ageing Res Rev 48:40–50
pubmed: 30300712
Thai PN et al (2019) Mitochondrial quality control in aging and heart failure: influence of ketone bodies and mitofusin-stabilizing peptides. Front Physiol 10:382
pubmed: 31024341 pmcid: 6467974
Wang K et al (2013) Thioredoxin reductase was nitrated in the aging heart after myocardial ischemia/reperfusion. Rejuvenation Res 16(5):377–385
pubmed: 23802942 pmcid: 3804317
Kwak H-B (2013) Effects of aging and exercise training on apoptosis in the heart. J Exerc Rehabil 9(2):212
pubmed: 24278863 pmcid: 3836520
Zhang R et al (2020) Mitophagy in cardiovascular homeostasis. Mech Ageing De 188:111245
No M-H et al (2020) Aging promotes mitochondria-mediated apoptosis in rat hearts. Life 10(9):178
pubmed: 32899456 pmcid: 7555313
Luo H et al (2020) A healthy heart and a healthy brain: looking at mitophagy. Front Cell Dev Biol 8:294
pubmed: 32435642 pmcid: 7218083
Ma L et al (2017) Restoring pharmacologic preconditioning in the aging heart: role of mitophagy/autophagy. J Gerontol: Series A 72(4):489–498
Chen G, Kroemer G, Kepp O (2020) Mitophagy: an emerging role in aging and age-associated diseases. Front Cell Dev Biol 8:200
pubmed: 32274386 pmcid: 7113588
Wei X et al (2021) Decreased dynamin-related protein 1-related mitophagy induces myocardial apoptosis in the aging heart. Acta Biochim Biophys Sin 53(10):1354–1366
pubmed: 34532739
Tong M, Zablocki D, Sadoshima J (2020) The role of Drp1 in mitophagy and cell death in the heart. J Mol Cell Cardiol 142:138–145
pubmed: 32302592 pmcid: 7545744
Tong M and J, et al (2016) Mitochondrial autophagy in car-diomyopathy. Curr Opin Genet Dev 38:8–15
pubmed: 27003723 pmcid: 5028232
Ren XC et al (2017) Resveratrol ameliorates mitochondrial elongation via Drp1/Parkin/PINK1 signaling in senescent-like cardiomyocytes. Oxid Med Cell Longev
Tsubouchi K et al (2018) PINK1-PARK2-mediated mitophagy in COPD and IPF pathogeneses. Inflamm Regen 38
Ashrafi G et al (2013) The Pathways of Mitophagy for Quality Control and Clearance of Mitochondria. Cell Death Differ 20(1):31–42
pubmed: 22743996
Nardin M et al (2016) Vitamin D status, diabetes mellitus and coronary artery disease in patients undergoing coronary angiography. Atherosclerosis 250 114 – 21
Seker T et al (2015) Lower serum 25-hydroxyvitamin D level is associated with impaired myocardial performance and left ventricle hypertrophy in newly diagnosed hypertensive patients. Anatol J Cardiol 15(9):744
pubmed: 25592096
Hazique M et al (2022) A study of vitamin D and its correlation with severity and complication of congestive heart failure: a systematic review. Cureus 6 14(9):28873
Witte KK et al (2016) Effects of vitamin D on cardiac function in patients with chronic HF: the VINDICATE study. J Am Coll Cardiol 67(22):2593–2603
pubmed: 27058906 pmcid: 4893154
Norman P et al (2014) Vitamin D and cardiovascular disease. Circ Re 17 114(2) 379 – 93
Greco D et al (2018) Vitamin D replacement ameliorates serum lipoprotein functions, adipokine profile and subclinical atherosclerosis in pre-menopausal women. Nutr Metab Cardiovasc Dis 28(8):822–882
pubmed: 29954641
Stokić E et al (2015) Vitamin D and dysfunctional adipose tissue in obesity. Angiology 66(7):613–618
pubmed: 25053676
Dehghani A et al (2019) Resveratrol and 1, 25-dihydroxyvitamin D co-administration protects the heart against D-galactose-induced aging in rats: evaluation of serum and cardiac levels of klotho. Aging Clin Exp Res 31 1195 – 205
Jeremy M, Gurusubramanian G, Roy VK (2019) Vitamin D3 regulates apoptosis and proliferation in the testis of D-galactose-induced aged rat model. Sci Rep 9(1):14103
pubmed: 31575929 pmcid: 6773724
Liu J et al (2020) Taurine protects against cardiac dysfunction induced by pressure overload through SIRT1–p53 activation. Chem Biol Interact 317:108972
pubmed: 32017914
Matthews D, Mittleman G (2017) Age-dependent effects of chronic intermittent ethanol treatment: gross motor behavior and body weight in aged, adult and adolescent rats. Neurosci Lett 14:657:146–150
Husain K et al (2014) Alcohol-induced hypertension: mechanism and prevention. World J Cardio 6(5):245–252
Liu D et al (2019) Heat shock factor 1-mediated transcription activation of Omi/HtrA2 induces myocardial mitochondrial apoptosis in the aging heart. Aging 11(20):8982
pubmed: 31627188 pmcid: 6834417
Pereira RM et al (2018) Protective molecular mechanisms of clusterin against apoptosis in cardiomyocytes. Heart Fail Rev 23:123–129
pubmed: 28948410
Qiu Z et al (2019) The role of myocardial mitochondrial quality control in heart failure. Front Pharmacol 10:1404
pubmed: 31866862 pmcid: 6910121
Ryu D et al (2016) Urolithin A induces mitophagy and prolongs lifespan in C. elegans and increases muscle function in rodents. Nat Med 22(8):879–888
pubmed: 27400265
Hasnat M et al (2019) Drp1-associated mitochondrial dysfunction and mitochondrial autophagy: a novel mechanism in triptolide-induced hepatotoxicity. Cell Biol Toxicol 35:267–280
pubmed: 30542779
Wang DB et al (2013) Declines in Drp1 and parkin expression underlie DNA damage-induced changes in mitochondrial length and neuronal death. J Neurosci Res 33(41):357–365
Li Y, Liu X (2018) Novel insights into the role of mitochondrial fusion and fission in cardiomyocyte apoptosis induced by ischemia/reperfusion. J Cell Physiol 233(8):5589–5597
pubmed: 29528108
Tong Met al et al (2023) Distinct roles of DRP1 in conventional and alternative mitophagy in obesity cardiomyopathy. Circ Res 133(1):6–21
Shirakabe A et al (2015) Drp1-dependent mitochondrial autophagy plays a protective role in response to pressure overload Induced mitochondrial dysfunction and heart failure. Circulation 132:17574
Zhang Y et al (2020) Drp1-dependent mitochondrial fission contributes to cr (VI)-induced mitophagy and hepatotoxicity. Ecotoxicol Environ Saf 203:110928
pubmed: 32888618
Buhlman L et al (2014) Functional interplay between parkin and Drp1 in mitochondrial fission and clearance. Biochim Biophys Acta Mol Cell Res 1843(9):2012–2026
Morales PE et al (2020) Emerging role of mitophagy in cardiovascular physiology and pathology. Mol Aspects Med 71:100822
pubmed: 31587811
Lin X-H et al (2020) Suppressing DRP1-mediated mitochondrial fission and mitophagy increases mitochondrial apoptosis of hepatocellular carcinoma cells in the setting of hypoxia. Oncogenesis 9(7):67
pubmed: 32661251 pmcid: 7359348
Bakula D and M (2020) Scheibye-Knudsen, MitophAging: mitophagy in aging and disease. Front Cell Dev Biol 8:239
pubmed: 32373609 pmcid: 7179682
Song M et al (2015) Interdependence of parkin-mediated mitophagy and mitochondrial fission in adult mouse hearts. Circ Res 117(4):346–351
pubmed: 26038571 pmcid: 4522211
Wan Q et al (2018) Mir-499-5p attenuates mitochondrial fission and cell apoptosis via P21 in Doxorubicin Cardiotoxicity. Front Genet 9:734
pubmed: 30719033
Ham SJ et al (2020) Decision between Mitophagy and apoptosis by parkin via VDAC1 ubiquitination. Proc Natl Acad Sci 117(8):4281–4291
pubmed: 32047033 pmcid: 7049170
Ren X et al (2017) Resveratrol ameliorates mitochondrial elongation via Drp1/Parkin/PINK1 signaling in senescent-like cardiomyocytes. Oxid Med Cell Longev 2017:4175353
pubmed: 29201272 pmcid: 5671746
Wan M et al (2022) YQFM alleviated cardiac hypertrophy by apoptosis inhibition and autophagy regulation via PI3K/AKT/mTOR pathway. J Ethnopharmacol 1(285):114835
Reddy AM et al (2022) Pivotal role of vitamin D in mitochondrial health, cardiac function, and human reproduction. EXCLI j 21:967
Lee T-L et al (2020) Vitamin D attenuates ischemia/reperfusion-induced cardiac injury by reducing mitochondrial fission and mitophagy. Front Pharmacol 11:604700
pubmed: 33362559 pmcid: 7758530
Milazzo V et al (2017) Vitamin D and acute myocardial infarction. World J Cardiol 9(1):14
pubmed: 28163832 pmcid: 5253190
Lee KJ et al (2021) Cytoprotective effect of vitamin d on doxorubicin-induced cardiac toxicity in triple negative breast cancer. Int J Mol Sci 22(14):7439
pubmed: 34299059 pmcid: 8305038
Latic N, Erben RG (2020) Vitamin D and cardiovascular disease, with emphasis on hypertension, atherosclerosis, and heart failure. Int J Mol Sci 21(18):6483
pubmed: 32899880 pmcid: 7555466
Ferder Met al et al (2013) The world pandemic of vitamin D deficiency could possibly be explained by cellular inflammatory response activity induced by the renin-angiotensin system. Am J Physiol Cell Physiol 304(11):1027–1039
Pilz S et al (2016) Vitamin D and cardiovascular disease prevention. Nat Rev Cardiol 13(7):404–417
pubmed: 27150190
Chen S et al (2011) Cardiomyocyte-specific deletion of the vitamin D receptor gene results in cardiac hypertrophy. Circulation 124(17):1838–1847
pubmed: 21947295 pmcid: 4160312

Auteurs

Siamak Shahidi (S)

Department of Physiology, School of medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Department of Neuroscience, School of Sciences and Advanced Technology in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.

Khadijeh Ramezani-Aliakbari (K)

Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Alireza Komaki (A)

Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Department of Neuroscience, School of Sciences and Advanced Technology in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.

Iraj Salehi (I)

Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Department of Neuroscience, School of Sciences and Advanced Technology in Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.

Sayedpayam Hashemi (S)

Medical School, Hamadan University of Medical Sciences, Hamadan, Iran.

Sara Soleimani Asl (SS)

Anatomy Department, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran.

Parisa Habibi (P)

Department of Physiology, School of medicine, Hamadan University of Medical Sciences, Hamadan, Iran.
Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.

Fatemeh Ramezani-Aliakbari (F)

Department of Physiology, School of medicine, Hamadan University of Medical Sciences, Hamadan, Iran. F.ramezani@umsha.ac.ir.
Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran. F.ramezani@umsha.ac.ir.

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Classifications MeSH