[1] KURO-O M, MATSUMURA Y, AIZAWA H, et al. Mutation of the mouse klotho gene leads to a syndrome resembling ageing[J]. Nature, 1997, 390(6655): 45-51.[2] NAGAI T, YAMADA K, KIM H C, et al. Cognition impairment in the genetic model of aging klotho gene mutant mice: a role of oxidative stress [J]. Faseb J, 2003, 17(1): 50-52.[3] SHIOZAKI M, YOSHIMURA K, SHIBATA M, et al. Morphological and biochemical signs of age-related neurodegenerative changes in klotho mutant mice[J]. Neuroscience, 2008, 152(4): 924-941.[4] KUROSU H, YAMAMOTO M, CLARK J D, et al. Suppression of aging in mice by the hormone klotho[J]. Science, 2005, 309(5742): 1829-1833.[5] MATSUMURA Y, AIZAWA H, SHIRAKI-IIDA T, et al. Identification of the human klotho gene and its two transcripts encoding membrane and secreted klotho protein[J]. Biochemical and Biophysical Research Communications, 1998, 242(3): 626-630.[6] SHIRAKI-IIDA T, AIZAWA H, MATSUMURA Y, et al. Structure of the mouse klotho gene and its two transcripts encoding membrane and secreted protein[J]. FEBS Letters, 1998, 424(1-2): 6-10.[7] URAKAWA I, YAMAZAKI Y, SHIMADA T, et al. Klotho converts canonical FGF receptor into a specific receptor for FGF23[J]. Nature, 2006, 444(7120): 770-774.[8] CHANG Q, HOEFS S, VAN DER KEMP A W, et al. The beta-glucuronidase klotho hydrolyzes and activates the TRPV5 channel[J]. Science, 2005, 310(5747): 490-493.[9] CHA S K, ORTEGA B, KUROSU H, et al. Removal of sialic acid involving klotho causes cell-surface retention of TRPV5 channel via binding to galectin-1[J]. Proc Natl Acad Sci USA, 2008, 105(28): 9805-9810.[10] IMURA A, TSUJI Y, MURATA M, et al. alpha-Klotho as a regulator of calcium homeostasis[J]. Science, 2007, 316(5831): 1615-1618.[11] YAMAMOTO M, CLARK J D, PASTOR J V, et al. Regulation of oxidative stress by the anti-aging hormone klotho[J]. Journal of Biological Chemistry, 2005, 280(45): 38029-38034.[12] MAEKAWA Y, ISHIKAWA K, YASUDA O, et al. Klotho suppresses TNF-alpha-induced expression of adhesion molecules in the endothelium and attenuates NF-kappaB activation[J]. Endocrine, 2009, 35(3): 341-346.[13] LIU F, WU S, REN H, et al. Klotho suppresses RIG-I-mediated senescence-associated inflammation[J]. Nature Cell Biology, 2011, 13(3): 254-262.[14] MORENO J A, IZQUIERDO M C, SANCHEZ-NINO M D, et al. The inflammatory cytokines TWEAK and TNFalpha reduce renal klotho expression through NFkappaB[J]. Journal of the American Society of Nephrology, 2011, 22(7): 1315-1325.[15] ZHAO Y, BANERJEE S, DEY N, et al. Klotho depletion contributes to increased inflammation in kidney of the db/db mouse model of diabetes via RelA (serine)536 phosphorylation[J]. Diabetes, 2011, 60(7): 1907-1916.[16] FENG R, WANG H, WANG J, et al. Forebrain degeneration and ventricle enlargement caused by double knockout of Alzheimer’s presenilin-1 and presenilin-2[J]. Proc Natl Acad Sci USA, 2004, 101(21): 8162-8167.[17] SAURA C A, CHOI S Y, BEGLOPOULOS V, et al. Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration[J]. Neuron, 2004, 42(1): 23-36.[18] BEGLOPOULOS V, SUN X, SAURA C A, et al. Reduced beta-amyloid production and increased inflammatory responses in presenilin conditional knock-out mice[J]. Journal of Biological Chemistry, 2004, 279(45): 46907-46914.[19] JIANG X, ZHANG D, SHI J, et al. Increased inflammatory response both in brain and in periphery in presenilin 1 and presenilin 2 conditional double knock-out mice[J]. Journal of Alzheimers Disease, 2009, 18(3): 515-523.[20] ZHU M, GU F, SHI J, et al. Increased oxidative stress and astrogliosis responses in conditional double-knockout mice of Alzheimer-like presenilin-1 and presenilin-2[J]. Free Radical Biology and Medicine, 2008, 45(10): 1493-1499.[21] WANG D, YANG L, SU J, et al. Attenuation of neurodegenerative phenotypes in Alzheimer-like presenilin 1/presenilin 2 conditional double knockout mice by EUK1001, a promising derivative of xanomeline[J]. Biochemical and Biophysical Research Communications, 2011, 410(2): 229-234.[22] DUCE J A, PODVIN S, HOLLANDER W, et al. Gene profile analysis implicates klotho as an important contributor to aging changes in brain white matter of the rhesus monkey[J]. Glia, 2008, 56(1): 106-117.[23] YAMAZAKI Y, IMURA A, URAKAWA I, et al. Establishment of sandwich ELISA for soluble alpha-klotho measurement: Age-dependent change of soluble alpha-klotho levels in healthy subjects[J]. Biochemical and Biophysical Research Communications, 2010, 398(3): 513-518.[24] KOH N, FUJIMORI T, NISHIGUCHI S, et al. Severely reduced production of klotho in human chronic renal failure kidney[J]. Biochemical and Biophysical Research Communications, 2001, 280(4): 1015-1020.[25] HU M C, KURO-O M, MOE O W. Secreted klotho and chronic kidney disease[J]. Advances in Experimental Medicine and Biology, 2012, 728: 126-157.[26] SUGIURA H, YOSHIDA T, TSUCHIYA K, et al. Klotho reduces apoptosis in experimental ischaemic acute renal failure[J]. Nephrology Dialysis Transplantation, 2005, 20(12): 2636-2645.[27] KOSAKAI A, ITO D, NIHEI Y, et al. Degeneration of mesencephalic dopaminergic neurons in klotho mouse related to vitamin D exposure[J]. Brain Research, 2011, 1382: 109-117.[28] LI H, WANG B, WANG Z, et al. Soluble amyloid precursor protein (APP) regulates transthyretin and Klotho gene expression without rescuing the essential function of APP[J]. Proc Natl Acad Sci USA, 2010, 107(40): 17362-17367.[29] 〖JP+3〗WU P, SHEN Q, DONG S, et al. Calorie restriction ameliorates neurodegenerative phenotypes in forebrain-specific presenilin-1 and presenilin-2 double knockout mice[J]. Neurobiology of Aging, 2008, 29(10): 1502-1511.〖JP〗[30] DONG S, LI C, WU P, et al. Environment enrichment rescues the neurodegenerative phenotypes in presenilins-deficient mice[J]. European Journal of Neuroscience, 2007, 26(1): 101-112.[31] BERNDT T, KUMAR R. Phosphatonins and the regulation of phosphate homeostasis[J]. Annual Review of Physiology, 2007, 69: 341-359.[32] KUROSU H, OGAWA Y, MIYOSHI M, et al. Regulation of fibroblast growth factor-23 signaling by klotho[J]. Journal of Biological Chemistry, 2006, 281(10): 6120-6123.[33] TSUJIKAWA H, KUROTAKI Y,FUJIMORI T, et al. Klotho, a gene related to a syndrome resembling human premature aging, functions in a negative regulatory circuit of vitamin D endocrine system[J]. Molecular Endocrinology, 2003, 17(12): 2393-2403.[34] BROWNSTEIN C A, ADLER F, NELSON-WILLIAMS C, et al. A translocation causing increased alpha-klotho level results in hypophosphatemic rickets and hyperparathyroidism[J]. Proc Natl Acad Sci USA, 2008, 105(9): 3455-3460.[35] KESTENBAUM B, SAMPSON J N, RUDSER K D, et al. Serum phosphate levels and mortality risk among people with chronic kidney disease[J]. Journal of the American Society of Nephrology, 2005, 16(2): 520-528.[36] RAKUGI H, MATSUKAWA N, ISHIKAWA K, et al. Anti-oxidative effect of klotho on endothelial cells through cAMP activation[J]. Endocrine, 2007, 31(1): 82-87.[37] GU F, ZHU M, SHI J, et al. Enhanced oxidative stress is an early event during development of Alzheimer-like pathologies in presenilin conditional knock-out mice[J]. Neuroscience Letters, 2008, 440(1): 44-48.[38] HERREMAN A, HARTMANN D, ANNAERT D, et al. Presenilin 2 deficiency causes a mild pulmonary phenotype and no changes in amyloid precursor protein processing but enhances the embryonic lethal phenotype of presenilin 1 deficiency[J]. Proc Natl Acad Sci USA, 1999, 96(21): 11872-11877. |