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| Research progress of CD38 in cardiovascular and cerebrovascular diseases |
| WANG Yanying JIAO Lei ZHANG Ying |
| Department of Pharmacology, College of Pharmacy, Harbin Medical University, Heilongjiang Province, Harbin 150081, China |
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Abstract Cardiovascular and cerebrovascular diseases seriously affect people′s health and life in today′s society. They mainly refer to ischemic or hemorrhagic diseases of heart, brain and systemic tissues caused by hyperlipidemia, atherosclerosis and hypertension. CD38 is a type Ⅱ transmembrane glycoprotein located on the membrane and its functional structure is relatively complex. Current studies have found that the more complex functions of CD38 make it play an important role in cardiovascular and cerebrovascular diseases. Based on the latest domestic and foreign reports, this article briefly reviews the role of CD38 in different cardiovascular and cerebrovascular diseases.
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[1] Malavasi F，Deaglio S，Funaro A，et al. Evolution and function of the ADP ribosyl cyclase/CD38 gene family in physiology and pathology [J]. Physiol Rev，2008，88（3）：841-886.
[2] Aarhus R，Graeff RM，Dickey DM，et al. ADP-ribosyl cyclase and CD38 catalyze the synthesis of a calcium-mobilizing metabolite from NADP [J]. J Biol Chem，1995，270（51）：30327-30333.
[3] Malavasi F，Funaro A，Roggero S，et al. Human CD38：a glycoprotein in search of a function [J]. Immunol Today，1994，15（3）：95-97.
[4] Quarona V，Zaccarello G，Chillemi A，et al. CD38 and CD157：a long journey from activation markers to multifunctional molecules [J]. Cytometry B Clin Cytom，2013，84（4）：207-217.
[5] Jackson DG，Bell JI. Isolation of a cDNA encoding the human CD38 （T10） molecule，a cell surface glycoprotein with an unusual discontinuous pattern of expression during lymphocyte differentiation [J]. J Immunol，1990，144（7）：2811-2815.
[6] Howard M，Grimaldi JC，Bazan JF，et al. Formation and hydrolysis of cyclic ADP-ribose catalyzed by lymphocyte antigen CD38 [J]. Science，1993，262（5136）：1056-1059.
[7] Levy D，Garrison RJ，Savage DD，et al. Prognostic implications of echocardiographically determined left ventricular mass in the Framingham heart study [J]. N Engl J Med，1990，323（24）：1706-1707.
[8] Barbosa MT，Soares SM，Novak CM，et al. The enzyme cd38 is necessary for the development of diet-induced obesity [J]. FASEB J，2007，21（13）：3629-3639.
[9] Guan XH，Hong X，Zhao N，et al. Cd38 promotes angiotensin ii-induced cardiac hypertrophy [J]. J Cell Mol Med，2017， 21（8）：1492-1502.
[10] Frank A，Bonney M，Bonney S，et al. Myocardial ischemia reperfusion injury：from basic science to clinical bedside [J]. Semin Cardiothorac Vasc Anesth，2012，16（3）：123-132.
[11] Ge Y，Jiang W，Gan L，et al. Mouse embryonic fibroblasts from CD38 knockout mice are resistant to oxidative stresses through inhibition of reactive oxygen species production and Ca2+ overload [J]. Biochem Biophy Res Commun，2010，399（2）：167-172.
[12] Guan XH，Liu XH，Hong X，et al. CD38 deficiency protects the heart from ischemia/reperfusion injury through activating SIRT1/FOXOs-mediated antioxidative stress pathway [J]. Oxid Med Cell Longev，2016，2016：7410257.
[13] James B，Nikhil R，Yasmin AA，et al. Inhibition of CD38 with the thiazoloquin（az）olin（on）e 78c protects the heart against postischemic [J]. Injury J Pharmacol Exp Ther，2019，369（1）：55-64.
[14] Wang LF，Huang CC，Xiao YF，et al. CD38 deficiency protects heart from high fat diet-induced oxidative stressvia activating Sirt3/FOXO3 pathway [J]. Cell Physiol Biochem，2018，48（6）：2350-2363.
[15] Lopez-Otin C，Blasco MA，Partridge L，et al. The hallmarks of aging [J]. Cell，2013，153（6）：1194-1217.
[16] Aksoy P，White TA，Thompson M，et al. Regulation of intracellular levels of NAD：a novel role for CD38 [J]. Biochem Biophys Res Commun，2006，345（4）：1386-1392.
[17] Camacho-Pereira J，Tarrago MG，Chini CCS，et al. CD38 dictates age-related nad decline and mitochondrial dysfunction through an SIRT3-dependent mechanism [J]. Cell Metab，2016，23（6）：1127-1139.
[18] Tarrago MG，Chini CCS，Kanamori KS，et al. A potent and specific cd38 inhibitor ameliorates age-related metabolic dysfunction by reversing tissue NAD+ decline [J]. Cell Metab，2018，27（5）：1081-1095.
[19] Wang LF，Cao Q，Wen K，et al. CD38 deficiency alleviates d-galactose-induced myocardial cell senescence through NAD+/sirt1 signaling pathway [J]. Front Physiol，2019，10：1125.
[20] Aaron L，Ji HP，Nina K，et al. CD38 knockout mice show significant protection against ischemic brain damage despite high level poly-ADP-ribosylation [J]. Neurochem Res，2017，42（1）：283-293.
[21] Choe CU，Lardong K，Gelderblom M，et al. CD38 exacerbates focal cytokine production，postischemic inflammation and brain injury after focal cerebral ischemia [J]. PLoS One，2011，6（5）：e19046.
[22] Zhang F，Xu M，Han WQ，et al. Reconstitution of lysosomal NAADP-TRP-ML1 signaling pathway and its function in TRP-ML1-/- cells [J]. Am J Physiol Cell Physiol，2011，301（2）：C421-C430.
[23] Johnson JD，Misler S. Nicotinic acid-adenine dinucleotide phosphate-sensitive calcium stores initiate insulin signaling in human beta cells [J]. Proc Natl Acad Sci USA，2002，99（22）：14566-14571.
[24] Lee HC. Physiological functions of cyclic ADP-ribose and NAADP as calcium messengers [J]. Annu Rev Pharmacol Toxicol，2001，41：317-345.
[25] Zhang F，Xia M，Li PL. Lysosome-dependent Ca2+ release response to Fas activation in coronary arterial myocytes through NAADP：evidence from CD38 gene knockouts [J]. Am J Physiol Cell Physiol，2010，298（5）：C1209-C1216.
[26] Yamasaki M，Masgrau R，Morgan AJ，et al. Organelle selection determines agonist-specific Ca2+ signals in pancreatic acinar and beta cells [J]. J Biol Chem，2004，279（8）：7234-7240.
[27] Aarhus R，Graeff RM，Dickey DM，et al. ADP-ribosyl cyclase and CD38 catalyze the synthesis of a calcium-mobilizing metabolite from NADP [J]. J Biol Chem，1995，270（51）：30327-30333.
[28] Zhang F，Zhang G，Zhang AY，et al. Production of NAADP and its role in Ca2+ mobilization associated with lysosomes in coronary arterial myocytes [J]. Am J Physiol Heart Circ Physiol，2006，291（1）：H274-H282.
[29] Rah SY，Mushtaq M，Nam TS，et al. Generation of cyclic ADP-ribose and nicotinic acid adenine dinucleotide phosphate by CD38 for Ca2+ signaling in interleukin-8-treated lymphokine-activated killer cells [J]. J Biol Chem，2010，285（28）：21877-21887.
[30] Cosker F，Cheviron N，Yamasaki M，et al. The ecto-enzyme CD38 is a nicotinic acid adenine dinucleotide phosphate （NAADP） synthase that couples receptor activation to Ca2+ mobilization from lysosomes in pancreatic acinar cells [J]. J Biol Chem，2010，285（49）：38251-38259.
[31] Xu XY，Yuan XX，Li NJ，et al. Lysosomal cholesterol accumulation in macrophages leading to coronary atherosclerosis in CD38-/- mice [J]. J Cell Mol Med，2016，20（6）：1001-1013. |
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