The involvement of protein kinases in the cardioprotective effect of chronic hypoxia
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články, přehledy
PubMed
33129243
PubMed Central
PMC8549881
DOI
10.33549/physiolres.934439
PII: 934439
Knihovny.cz E-zdroje
- MeSH
- chronická nemoc MeSH
- hypoxie enzymologie MeSH
- kardiotonika farmakologie MeSH
- lidé MeSH
- nemoci srdce enzymologie etiologie prevence a kontrola MeSH
- proteinkinasy metabolismus MeSH
- zvířata MeSH
- Check Tag
- lidé MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- přehledy MeSH
- Názvy látek
- kardiotonika MeSH
- proteinkinasy MeSH
The purpose of this review is to analyze the involvement of protein kinases in the cardioprotective mechanism induced by chronic hypoxia. It has been reported that chronic intermittent hypoxia contributes to increased expression of the following kinases in the myocardium: PKCdelta, PKCalpha, p-PKCepsilon, p-PKCalpha, AMPK, p-AMPK, CaMKII, p-ERK1/2, p-Akt, PI3-kinase, p-p38, HK-1, and HK-2; whereas, chronic normobaric hypoxia promotes increased expression of the following kinases in the myocardium: PKCepsilon, PKCbetaII, PKCeta, CaMKII, p-ERK1/2, p-Akt, p-p38, HK-1, and HK-2. However, CNH does not promote enhanced expression of the AMPK and JNK kinases. Adaptation to hypoxia enhances HK-2 association with mitochondria and causes translocation of PKCdelta, PKCbetaII, and PKCeta to the mitochondria. It has been shown that PKCdelta, PKCepsilon, ERK1/2, and MEK1/2 are involved in the cardioprotective effect of chronic hypoxia. The role of other kinases in the cardioprotective effect of adaptation to hypoxia requires further research.
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ANDERSON M. Calmodulin kinase signaling in heart: an intriguing candidate target for therapy of myocardial dysfunction and arrhythmias. Pharmacol Ther. 2005;106:39–55. doi: 10.1016/j.pharmthera.2004.11.002. PubMed DOI
ENDOH M. The effects of various drugs on the myocardial inotropic response. Gen Pharmacol. 1995;26:1–31. doi: 10.1016/0306-3623(94)00144-C. PubMed DOI
GAO Q, HU J, HU J, YU Y, YE H, LI Z, GUAN S. Calcium activated potassium channel and protein kinase C participate in the cardiac protection of remote post conditioning. Pak J Pharm Sci. 2013;26:285–90. PubMed
GU S, HUA H, GUO X, JIA Z, ZHANG Y, MASLOV LN, ZHANG X, MA H. PGC-1α participates in the protective effect of chronic intermittent hypobaric hypoxia on cardiomyocytes. Cell Physiol Biochem. 2018;50:1891–1902. doi: 10.1159/000494869. PubMed DOI
HE S, LIU S, WU X, XIN M, DING S, XIN D, OUYANG H, ZHANG J. Protective role of downregulated MLK3 in myocardial adaptation to chronic hypoxia. J Physiol Biochem. 2016;73:371–380. doi: 10.1007/s13105-017-0561-5. PubMed DOI
HEIDBREDER M, NAUMANN A, TEMPEL K, DOMINIAK P, DENDORFER A. Remote vs. ischaemic preconditioning: the differential role of mitogen-activated protein kinase pathways. Cardiovasc Res. 2008;78:108–115. doi: 10.1093/cvr/cvm114. PubMed DOI
HERMANN R, MARINA PRENDES MG, TORRESIN ME, VÉLEZ D, SAVINO EA, VARELA A. Effects of the AMP-activated protein kinase inhibitor compound C on the postconditioned rat heart. J Physiol Sci. 2012;62:333–341. doi: 10.1007/s12576-012-0209-8. PubMed DOI PMC
HEUSCH G. Molecular basis of cardioprotection: signal transduction in ischemic pre-, post-, and remote conditioning. Circ Res. 2015;116:674–699. doi: 10.1161/CIRCRESAHA.116.305348. PubMed DOI
HLAVÁČKOVÁ M, KOŽICHOVÁ K, NECKÁŘ J, KOLÁŘ F, MUSTERS RJ, NOVÁK F, NOVÁKOVÁ O. Up-regulation and redistribution of protein kinase C-δ in chronically hypoxic heart. Mol Cell Biochem. 2010;345:271–282. doi: 10.1007/s11010-010-0581-8. PubMed DOI
HLAVÁČKOVÁ M, NECKÁR J, JEZKOVÁ J, BALKOVÁ P, STANKOVÁ B, NOVÁKOVÁ O, KOLÁR F, NOVÁK F. Dietary polyunsaturated fatty acids alter myocardial protein kinase C expression and affect cardioprotection induced by chronic hypoxia. Exp Biol Med (Maywood) 2007;232:823–832. PubMed
HOLZEROVA K, HLAVÁČKOVÁ M, ŽURMANOVÁ J, BORCHERT G, NECKÁŘ J, KOLÁŘ F, NOVÁK F, NOVÁKOVÁ O. Involvement of PKCε in cardioprotection induced by adaptation to chronic continuous hypoxia. Physiol Res. 2015;64:191–201. doi: 10.33549/physiolres.932860. PubMed DOI
INSERTE J, HERNANDO V, VILARDOSA Ú, ABAD E, PONCELAS-NOZAL M, GARCIA-DORADO D. Activation of cGMP/protein kinase G pathway in postconditioned myocardium depends on reduced oxidative stress and preserved endothelial nitric oxide synthase coupling. J Am Heart Assoc. 2013;2:e005975. doi: 10.1161/JAHA.112.005975. PubMed DOI PMC
JONASSEN AK, SACK MN, MJOS OD, YELLON DM. Myocardial protection by insulin at reperfusion requires early administration and is mediated via Akt and p70s6 kinase cell-survival signaling. Circ Res. 2001;89:1191–1198. doi: 10.1161/hh2401.101385. PubMed DOI
KHALIULIN I, CLARKE SJ, LIN H, PARKER J, SULEIMAN MS, HALESTRAP AP. Temperature preconditioning of isolated rat hearts-a potent cardioprotective mechanism involving a reduction in oxidative stress and inhibition of the mitochondrial permeability transition pore. J Physiol. 2007;581:1147–1161. doi: 10.1113/jphysiol.2007.130369. PubMed DOI PMC
KOHUTOVA J, ELSNICOVA B, HOLZEROVA K, NECKAR J, SEBESTA O, JEZKOVA J, VECKA M, VEBR P, HORNIKOVA D, SZEIFFOVA BACOVA B, EGAN BENOVA T, HLAVACKOVA M, TRIBULOVA N, KOLAR F, NOVAKOVA O, ZURMANOVA JM. Anti-arrhythmic cardiac phenotype elicited by chronic intermittent hypoxia is associated with alterations in connexin-43 expression, phosphorylation, and distribution. Front Endocrinol (Lausanne) [Internet] 2019;9:1–10. doi: 10.3389/fendo.2018.00789. PubMed DOI PMC
KOLAR D, GRESIKOVA M, WASKOVA-ARNOSTOVA P, ELSNICOVA B, KOHUTOVA J, HORNIKOVA D, VEBR P, NECKAR J, BLAHOVA T, KASPAROVA D, NOVOTNY J, KOLAR F, NOVAKOVA O, ZURMANOVA JM. Adaptation to chronic continuous hypoxia potentiates Akt/HK2 anti-apoptotic pathway during brief myocardial ischemia/reperfusion insult. Mol Cell Biochem. 2017;432:99–108. doi: 10.1007/s11010-017-3001-5. PubMed DOI
KOLAR F, JEZKOVÁ J, BALKOVÁ P, BREH J, NECKÁR J, NOVÁK F, NOVÁKOVÁ O, TOMÁSOVÁ H, SRBOVÁ M, OST’ÁDAL B, WILHELM J, HERGET J. Role of oxidative stress in PKC-δ upregulation and cardioprotection induced by chronic intermittent hypoxia. Am J Physiol Heart Circ Physiol. 2007;292:H224–H230. doi: 10.1152/ajpheart.00689.2006. PubMed DOI
KOLAR F, OSTÁDAL B. Molecular mechanisms of cardiac protection by adaptation to chronic hypoxia. Physiol Res. 2004;53:S3–13. PubMed
LANGE M, SMUL TM, BLOMEYER CA, REDEL A, KLOTZ KN, ROEWER N, KEHL F. Role of the beta1-adrenergic pathway in anesthetic and ischemic preconditioning against myocardial infarction in the rabbit heart in vivo. Anesthesiology. 2006;105:503–510. doi: 10.1097/00000542-200609000-00014. PubMed DOI
LARSEN KO, LYGREN B, SJAASTAD I, KROBERT KA, ARNKVAERN K, FLORHOLMEN G, LARSEN AK, LEVY FO, TASKÉN K, SKJØNSBERG OH, CHRISTENSEN G. Diastolic dysfunction in alveolar hypoxia: a role for interleukin-18-mediated increase in protein phosphatase 2A. Cardiovasc Res. 2008;80:47–54. doi: 10.1093/cvr/cvn180. PubMed DOI
LI X, LIU Y, MA H, GUAN Y, CAO Y, TIAN Y, ZHANG Y. Enhancement of glucose metabolism via PGC-1α participates in the cardioprotection of chronic intermittent hypobaric hypoxia. Front Physiol. 2016;7:1–8. doi: 10.3389/fphys.2016.00219. PubMed DOI PMC
LING H, GRAY CB, ZAMBON AC, GRIMM M, GU Y, DALTON N, PURCELL NH, PETERSON K, BROWN JH. CaMKIIδ mediates myocardial ischemia/reperfusion injury through nuclear factor-κB. Circ Res. 2013;112:935–944. doi: 10.1161/CIRCRESAHA.112.276915. PubMed DOI PMC
LIU J, CHANG F, LI F, FU H, WANG J, ZHANG S, ZHAO J, YIN D. Palmitate promotes autophagy and apoptosis through ROS-dependent JNK and p38 MAPK. Biochem Biophys Res Commun. 2015;463:262–267. doi: 10.1016/j.bbrc.2015.05.042. PubMed DOI
MA HJ, LI Q, MA HJ, GUAN Y, SHI M, YANG J, LI DP, ZHANG Y. Chronic intermittent hypobaric hypoxia ameliorates ischemia/reperfusion-induced calcium overload in heart via Na+/Ca2+ exchanger in developing rats. Cell Physiol Biochem. 2014;34:313–324. doi: 10.1159/000363001. PubMed DOI
MAJEWSKI N, NOGUEIRA V, BHASKAR P, COY PE, SKEEN JE, GOTTLOB K, CHANDEL NS, THOMPSON CB, ROBEY RB, HAY N. Hexokinase-mitochondria interaction mediated by Akt is required to inhibit apoptosis in the presence or absence of Bax and Bak. Mol Cell. 2004;16:819–830. doi: 10.1016/j.molcel.2004.11.014. PubMed DOI
McCARTHY J, LOCHNER A, OPIE LH, SACK MN, ESSOP MF. PKCε promotes cardiac mitochondrial and metabolic adaptation to chronic hypobaric hypoxia by GSK3β inhibition. J Cell Physiol. 2011;226:2457–2468. doi: 10.1002/jcp.22592. PubMed DOI PMC
MEERSON FZ, USTINOVA EE, MANUKHINA EB. Prevention of cardiac arrhythmias by adaptation to hypoxia: regulatory mechanisms and cardiotropic effect. Biomed Biochim Acta. 1989;48:S83–S88. PubMed
MICOVA P, HAHNOVA K, HLAVACKOVA M, ELSNICOVA B, CHYTILOVA A, HOLZEROVA K, ZURMANOVA J, NECKAR J, KOLAR F, NOVAKOVA O, NOVOTNY J. Chronic intermittent hypoxia affects the cytosolic phospholipase A2α/cyclooxygenase 2 pathway via β2-adrenoceptor-mediated ERK/p38 stimulation. Mol Cell Biochem. 2016;423:151–163. doi: 10.1007/s11010-016-2833-8. PubMed DOI
MILANO G, MOREL S, BONNY C, SAMAJA M, von SEGESSER LK, NICOD P, VASSALLI G. A peptide inhibitor of c-Jun NH2-terminal kinase reduces myocardial ischemia-reperfusion injury and infarct size in vivo. Am J Physiol Heart Circ Physiol. 2007;292:H1828–H1835. doi: 10.1152/ajpheart.01117.2006. PubMed DOI
MILANO G, von SEGESSER LK, MOREL S, JONCIC A, BIANCIARDI P, VASSALLI G, SAMAJA M. Phosphorylation of phosphatidylinositol-3-kinase-protein kinase B and extracellular signal-regulated kinases 1/2 mediate reoxygenation-induced cardioprotection during hypoxia. Exp Biol Med (Maywood) 2010;235:401–410. doi: 10.1258/ebm.2009.009153. PubMed DOI
MILANO G, ABRUZZO PM, BOLOTTA A, MARINI M, TERRANEO L, RAVARA B, GORZA L, VITADELLO M, BURATTINI S, CURZI D, FALCIERI E, von SEGESSER LK, SAMAJA M. Impact of the phosphatidylinositide 3-kinase signaling pathway on the cardioprotection induced by intermittent hypoxia. PLoS ONE. 2013;8:e76659. doi: 10.1371/journal.pone.0076659. PubMed DOI PMC
MOHAMMED ABDUL KS, JOVANOVIĆ S, DU Q, SUKHODUB A, JOVANOVIĆ A. Mild hypoxia in vivo regulates cardioprotective SUR2A: A role for Akt and LDH. Biochim Biophys Acta - Mol Basis Dis, 2015;1852:709–719. doi: 10.1016/j.bbadis.2015.01.001. PubMed DOI PMC
MOCKRIDGE JW, MARBER MS, HEADS RJ. Activation of Akt during simulated ischemia/reperfusion in cardiac myocytes. Biochem Biophys Res Commun. 2000;270:947–952. doi: 10.1006/bbrc.2000.2522. PubMed DOI
MOREL OE, BUVRY A, LE CORVOISIER P, TUAL L, FAVRET F, LEÓN-VELARDE F, CROZATIER B, RICHALET JP. Effects of nifedipine-induced pulmonary vasodilatation on cardiac receptors and protein kinase C isoforms in the chronically hypoxic rat. Pflugers Arch. 2003;446:356–364. doi: 10.1007/s00424-003-1034-y. PubMed DOI
MOREL S, MILANO G, LUDUNGE KM, CORNO AF, SAMAJA M, FLEURY S, BONNY C, KAPPENBERGER L, von SEGESSER LK, VASSALLI G. Brief reoxygenation episodes during chronic hypoxia enhance posthypoxic recovery of LV function: role of mitogen-activated protein kinase signaling pathways. Basic Res Cardiol. 2006;101:336–345. doi: 10.1007/s00395-006-0596-1. PubMed DOI
NARYZHNAYA NV, KHALIULIN I, LISHMANOV YB, SULEIMAN MS, TSIBULNIKOV SY, KOLAR F, MASLOV LN. Participation of opioid receptors in the cytoprotective effect of chronic normobaric hypoxia. Physiol Res. 2019;68:245–253. doi: 10.33549/physiolres.933938. PubMed DOI
NARYZHNAYA NV, MASLOV LN, KHALIULIN IG, ZHANG Y, PEI JM, TSEPOKINA AV, KHUTORNAYA MV, KUTIKHIN AG, LISHMANOV YB. Chronic continuous normobaric hypoxia augments cell tolerance to anoxia/reoxygenation: the role of protein kinases. Ross Fiziol Zh Im I M Sechenova. 2016;102:1462–1471. PubMed
NECKAR J, MARKOVÁ I, NOVÁK F, NOVÁKOVÁ O, SZÁRSZOI O, OST’ÁDAL B, KOLÁR F. Increased expression and altered subcellular distribution of PKC-δ in chronically hypoxic rat myocardium: involvement in cardioprotection. Am J Physiol Heart Circ Physiol. 2005;288:H1566–H1572. doi: 10.1152/ajpheart.00586.2004. PubMed DOI
NEDVEDOVA I, KOLAR D, ELSNICOVA B, HORNIKOVA D, NOVOTNY J, KALOUS M, PRAVENEC M, NECKAR J, KOLAR F, ZURMANOVA JM. Mitochondrial genome modulates myocardial Akt/Glut/HK salvage pathway in spontaneously hypertensive rats adapted to chronic hypoxia. Physiol Genomics. 2018;50:532–541. doi: 10.1152/physiolgenomics.00040.2017. PubMed DOI
NEHRA S, BHARDWAJ V, KAR S, SARASWAT D. Chronic hypobaric hypoxia induces right ventricular hypertrophy and apoptosis in rats: therapeutic potential of nanocurcumin in improving adaptation. High Alt Med Biol. 2016;17:342–352. doi: 10.1089/ham.2016.0032. PubMed DOI
OKUBO S, TANABE Y, FUJIOKA N, TAKEDA K, TAKEKOSHI N. Differential activation of protein kinase C between ischemic and pharmacological preconditioning in the rabbit heart. Jpn J Physiol. 2003;53:173–80. doi: 10.2170/jjphysiol.53.173. PubMed DOI
PROKUDINA ES, NARYZHNAYA NV, MUKHOMEDZYANOV AV, GORBUNOV AS, ZHANG Y, YAGGI AS, TSIBULNIKOV SY, NESTEROV EA, LISHMANOV YB, SULEIMAN MS, OELTGEN PR, MASLOV LN. Effect of chronic continuous normobaric hypoxia on functional state of cardiac mitochondria and tolerance of isolated rat heart to ischemia and reperfusion: Role of μ and delta2. Physiol Res 30: 2019;68:909–920. doi: 10.33549/physiolres.933945. PubMed DOI
QUING M, GÖRLACH A, SCHUMACHER K, WÖLTJE M, VAZQUEZ-JIMENEZ JF, HESS J, SEGHAYE MC. The hypoxia-inducible factor HIF-1 promotes intramyocardial expression of VEGF in infants with congenital cardiac defects. Basic Res Cardiol. 2007;102:224–232. doi: 10.1007/s00395-007-0639-2. PubMed DOI
RAFIEE P, SHI Y, KONG X, PRITCHARD KA, TWEDDELL JS, LITWIN SB, MUSSATTO K, JAQUISS RD, SU J, BAKER JE. Activation of protein kinases in chronically hypoxic infant human and rabbit hearts: role in cardioprotection. Circulation. 2002;106:239–245. doi: 10.1161/01.CIR.0000022018.68965.6D. PubMed DOI
RAVINGEROVÁ T, MATEJÍKOVÁ J, NECKÁR J, ANDELOVÁ E, KOLÁR F. Differential role of PI3K/Akt pathway in the infarct size limitation and antiarrhythmic protection in the rat heart. Mol Cell Biochem. 2007;297:111–120. doi: 10.1007/s11010-006-9335-z. PubMed DOI
ROBINET A, HOIZEY G, MILLART H. PI 3-kinase, protein kinase C, and protein kinase A are involved in the trigger phase of beta1-adrenergic preconditioning. Cardiovasc Res. 2005;66:530–542. doi: 10.1016/j.cardiores.2005.02.010. PubMed DOI
ROSSELLO X, RIQUELME JA, DAVIDSON SM, YELLON DM. Role of PI3K in myocardial ischaemic preconditioning: mapping pro-survival cascades at the trigger phase and at reperfusion. J Cell Mol Med. 2018;22:926–935. doi: 10.1111/jcmm.13394. PubMed DOI PMC
SHOSHAN-BARMATZ V, ZAKAR M, ROSENTHAL K, ABU-HAMAD S. Key regions of VDAC1 functioning in apoptosis induction and regulation by hexokinase. Biochim Biophys Acta. 2009;1787:421–430. doi: 10.1016/j.bbabio.2008.11.009. PubMed DOI
STRNISKOVÁ M, RAVINGEROVÁ T, NECKÁR J, KOLÁR F, PASTOREKOVÁ S, BARANCÍK M. Changes in the expression and/or activation of regulatory proteins in rat hearts adapted to chronic hypoxia. Gen Physiol Biophys. 2006;25:25–41. PubMed
SUN HY, WANG NP, HALKOS M, KERENDI F, KIN H, GUYTON RA, VINTEN-JOHANSEN J, ZHAO ZQ. Postconditioning attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways. Apoptosis. 2006;11:1583–1593. doi: 10.1007/s10495-006-9037-8. PubMed DOI
SUGDEN PH, CLERK A. Regulation of the ERK subgroup of MAP kinase cascades through G protein-coupled receptors. Cell Signal. 9:337–51. doi: 10.1016/S0898-6568(96)00191-X. PubMed DOI
TANAKA T, SAOTOME M, KATOH H, SATOH T, HASAN P, OHTANI H, SATOH H, HAYASHI H, MAEKAWA Y. Glycogen synthase kinase-3β opens mitochondrial permeability transition pore through mitochondrial hexokinase II dissociation. J Physiol Sci. 2018;68:865–871. doi: 10.1007/s12576-018-0611-y. PubMed DOI PMC
TSIBULNIKOV SY, MASLOV LN, NARYZHNAYA NV, MA H, LISHMANOV YB, OELTGEN PR, GARLID K. Role of protein kinase C, PI3 kinase, tyrosine kinases, NO-synthase, KATP channels and MPT pore in the signaling pathway of the cardioprotective effect of chronic continuous hypoxia. Gen Physiol Biophys. 2018;37:537–547. doi: 10.4149/gpb_2018013. PubMed DOI
VIGANÒ A, VASSO M, CARETTI A, BRAVATÀ V, TERRANEO L, FANIA C, CAPITANIO D, SAMAJA M, GELFI C. Protein modulation in mouse heart under acute and chronic hypoxia. Proteomics. 2011;11:4202–4217. doi: 10.1002/pmic.201000804. PubMed DOI
WASKOVA-ARNOSTOVA P, ELSNICOVA B, KASPAROVA D, HORNIKOVA D, KOLAR F, NOVOTNY J, ZURMANOVA J. Cardioprotective adaptation of rats to intermittent hypobaric hypoxia is accompanied by the increased association of hexokinase with mitochondria. J Appl Physiol (1985) 2015;119:1487–1493. doi: 10.1152/japplphysiol.01035.2014. PubMed DOI
WEINBRENNER C, LIU GS, COHEN MV, DOWNEY JM. Phosphorylation of tyrosine 182 of p38 mitogen-activated protein kinase correlates with the protection of preconditioning in the rabbit heart. J Mol Cell Cardiol. 1997;29:2383–91. doi: 10.1006/jmcc.1997.0473. PubMed DOI
XIE S, DENG Y, PAN Y, REN J, JIN M, WANG Y, WANG Z, ZHU D, GUO X, YUAN X, SHANG J, LIU H. Chronic intermittent hypoxia induces cardiac hypertrophy by impairing autophagy through the adenosine 5′-monophosphate-activated protein kinase pathway. Arch Biochem Biophys. 2016;606:41–52. doi: 10.1016/j.abb.2016.07.006. PubMed DOI
XIE Y, ZHU WZ, ZHU Y, CHEN L, ZHOU ZN, YANG HT. Intermittent high altitude hypoxia protects the heart against lethal Ca2+ overload injury. Life Sci. 2004;76:559–772. doi: 10.1016/j.lfs.2004.09.017. PubMed DOI
YELLON DM, DOWNEY JM. Preconditioning the myocardium: from cellular physiology to clinical cardiology. Physiol Rev. 2003;83:1113–1151. doi: 10.1152/physrev.00009.2003. PubMed DOI
YEUNG HM, KRAVTSOV GM, NG KM, WONG TM, FUNG ML. Chronic intermittent hypoxia alters Ca2+ handling in rat cardiomyocytes by augmented Na+/Ca2+ exchange and ryanodine receptor activities in ischemia-reperfusion. Am J Physiol Cell Physiol. 2007;292:C2046–56. doi: 10.1152/ajpcell.00458.2006. PubMed DOI
ZENG C, LIANG B, JIANG R, SHI Y, DU Y. Protein kinase C isozyme expression in right ventricular hypertrophy induced by pulmonary hypertension in chronically hypoxic rats. Mol Med Rep. 2017;16:3833–3840. doi: 10.3892/mmr.2017.7098. PubMed DOI PMC
ZHANG H, LIU B, LI T, ZHU Y, LUO G, JIANG Y, TANG F, JIAN Z, XIAO Y. AMPK activation serves a critical role in mitochondria quality control via modulating mitophagy in the heart under chronic hypoxia. Int J Mol Med. 2018a;41:69–76. doi: 10.3892/ijmm.2017.3213. PubMed DOI PMC
ZHANG K, MA Z, WANG W, LIU R, ZHANG Y, YUAN M, LI G. Beneficial effects of tolvaptan on atrial remodeling induced by chronic intermittent hypoxia in rats. Cardiovasc Ther. 2018b;36:e12466. doi: 10.1111/1755-5922.12466. PubMed DOI
ZHAO PJ, PAN J, LI F, SUN K. Effects of chronic hypoxia on the expression of calmodulin and calcicum/calmodulin-dependent protein kinase II and the calcium activity in myocardial cells in young rats (In Chinese) Zhongguo Dang Dai Er Ke Za Zhi. 2008;10:381–385. PubMed
ZHAO YS, AN JR, YANG S, GUAN P, YU FY, LI W, LI JR, GUO Y, SUN ZM, JI ES. Hydrogen and oxygen mixture to improve cardiac dysfunction and myocardial pathological changes induced by intermittent hypoxia in rats. Oxid Med Cell Longev. 2019;2019:7415212. doi: 10.1155/2019/7415212. PubMed DOI PMC