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  1. Article ; Online: Calcium phosphate microcrystallopathy as a paradigm of chronic kidney disease progression.

    Kuro-O, Makoto

    Current opinion in nephrology and hypertension

    2023  Volume 32, Issue 4, Page(s) 344–351

    Abstract: Purpose of review: Calciprotein particles (CPP) are colloidal mineral-protein complexes mainly composed of solid-phase calcium phosphate and serum protein fetuin-A. CPP appear in the blood and renal tubular fluid after phosphate intake, playing critical ...

    Abstract Purpose of review: Calciprotein particles (CPP) are colloidal mineral-protein complexes mainly composed of solid-phase calcium phosphate and serum protein fetuin-A. CPP appear in the blood and renal tubular fluid after phosphate intake, playing critical roles in (patho)physiology of mineral metabolism and chronic kidney disease (CKD). This review aims at providing an update of current knowledge on CPP.
    Recent findings: CPP formation is regarded as a defense mechanism against unwanted growth of calcium phosphate crystals in the blood and urine. CPP are polydisperse colloids and classified based on the density and crystallinity of calcium phosphate. Low-density CPP containing amorphous (noncrystalline) calcium phosphate function as an inducer of FGF23 expression in osteoblasts and a carrier of calcium phosphate to the bone. However, once transformed to high-density CPP containing crystalline calcium phosphate, CPP become cytotoxic and inflammogenic, inducing cell death in renal tubular cells, calcification in vascular smooth muscle cells, and innate immune responses in macrophages.
    Summary: CPP potentially behave like a pathogen that causes renal tubular damage, chronic inflammation, and vascular calcification. CPP have emerged as a promising therapeutic target for CKD and cardiovascular complications.
    MeSH term(s) Humans ; alpha-2-HS-Glycoprotein/metabolism ; Calcium Phosphates/metabolism ; Renal Insufficiency, Chronic/complications ; Vascular Calcification/etiology ; Minerals/metabolism ; Phosphates/metabolism ; Calcium/metabolism
    Chemical Substances alpha-2-HS-Glycoprotein ; calcium phosphate (97Z1WI3NDX) ; Calcium Phosphates ; Minerals ; Phosphates ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2023-04-19
    Publishing country England
    Document type Review ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1151092-4
    ISSN 1473-6543 ; 1535-3842 ; 1062-4813 ; 1062-4821
    ISSN (online) 1473-6543 ; 1535-3842
    ISSN 1062-4813 ; 1062-4821
    DOI 10.1097/MNH.0000000000000890
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book: Endocrine FGFs and klothos

    Kuro-o, Makoto

    (Advances in experimental medicine and biology ; 728)

    2012  

    Abstract: Fibroblast growth factors (FGFs) have been recognized primarily as autocrine/paracrine factors that regulate embryonic development and organogenesis. However, recent studies have revealed that some FGFs function as endocrine factors and regulate various ...

    Author's details ed. by Makoto Kuro-o
    Series title Advances in experimental medicine and biology ; 728
    Collection
    Abstract "Fibroblast growth factors (FGFs) have been recognized primarily as autocrine/paracrine factors that regulate embryonic development and organogenesis. However, recent studies have revealed that some FGFs function as endocrine factors and regulate various metabolic processes in adulthood. Such FGFs, collectively called endocrine FGFs, are comprised of three members (FGF15/19, FGF21, and FGF23: FGF15 is the mouse ortholog of human FGF19). These endocrine FGFs share a common structural feature that enables the endocrine mode of action at the expense of the affinity to FGF receptors. To restore the affinity to FGF receptors in their target organs, the endocrine FGFs have designated the Klotho family of transmembrane proteins as obligate co-receptors. By expressing Klothos in a tissue-specific manner, this unique co-receptor system also enables the endocrine FGFs to specify their target organs among many tissues that express FGF receptors"--Provided by publisher
    Keywords Fibroblast Growth Factors / metabolism ; Glucuronidase / metabolism ; Endocrine System / metabolism ; Receptors, Fibroblast Growth Factor
    Language English
    Size XIX, 233 S. : Ill., graph. Darst.
    Publisher Springer u.a.
    Publishing place New York
    Publishing country United States
    Document type Book
    Note Includes bibliographical references and index
    HBZ-ID HT017147103
    ISBN 978-1-4614-0886-4 ; 1-4614-0886-5
    Database Catalogue ZB MED Medicine, Health

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  3. Article: Aging and FGF23-klotho system.

    Kuro-O, Makoto

    Vitamins and hormones

    2021  Volume 115, Page(s) 317–332

    Abstract: During the evolution of skeletons, vertebrates acquired the bone made of calcium phosphate. By keeping the extracellular fluid in a supersaturated condition regarding calcium and phosphate, vertebrates create the bone when and where they want simply by ... ...

    Abstract During the evolution of skeletons, vertebrates acquired the bone made of calcium phosphate. By keeping the extracellular fluid in a supersaturated condition regarding calcium and phosphate, vertebrates create the bone when and where they want simply by providing a cue for precipitation. To secure this strategy, a new endocrine system has evolved that strictly controls the extracellular phosphate concentration. In response to phosphate intake, fibroblast growth factor-23 (FGF23) is secreted from the bone and acts on the kidney through binding to its receptor Klotho to increase urinary phosphate excretion and maintain phosphate homeostasis. The FGF23-Klotho endocrine system, when disrupted, results in hyperphosphatemia and ectopic precipitation of calcium phosphate in mice and humans. In addition to disturbed phosphate homeostasis, mice lacking Klotho suffer from premature aging. They exhibit multiple organ atrophy, arteriosclerosis characterized by vascular calcification, cardiac hypertrophy, sarcopenia, cognition impairment, frailty, and a shortened life span associated with chronic non-infectious inflammation. Restoration of the phosphate balance by placing Klotho- or FGF23-deficient mice on low phosphate diet rescued them from the aging-like phenotypes, indicating that phosphate was responsible for the accelerated aging. The similar pathophysiology is universally observed in patients with chronic kidney disease (CKD), rendering advanced CKD a clinical model of accelerated aging. CKD patients bear colloidal nanoparticles containing calcium phosphate in the blood, which are termed calciprotein particles (CPPs). CPPs have the ability to induce cell damage and inflammation, potentially contributing to accelerated aging. Terrestrial vertebrates with the bone made of calcium phosphate may be destined to age due to ectopic calcium phosphate.
    MeSH term(s) Aging/physiology ; Animals ; Fibroblast Growth Factors/physiology ; Glucuronidase/physiology ; Humans ; Klotho Proteins ; Mice ; Phosphates/metabolism
    Chemical Substances Phosphates ; Fibroblast Growth Factors (62031-54-3) ; Glucuronidase (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31)
    Language English
    Publishing date 2021-01-25
    Publishing country United States
    Document type Journal Article
    ZDB-ID 201161-x
    ISSN 2162-2620 ; 0083-6729
    ISSN (online) 2162-2620
    ISSN 0083-6729
    DOI 10.1016/bs.vh.2020.12.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Klotho and calciprotein particles as therapeutic targets against accelerated ageing.

    Kuro-O, Makoto

    Clinical science (London, England : 1979)

    2021  Volume 135, Issue 15, Page(s) 1915–1927

    Abstract: The klotho gene, named after a Greek goddess who spins the thread of life, was identified as a putative 'ageing-suppressor' gene. Klotho-deficient mice exhibit complex ageing-like phenotypes including hypogonadism, arteriosclerosis (vascular ... ...

    Abstract The klotho gene, named after a Greek goddess who spins the thread of life, was identified as a putative 'ageing-suppressor' gene. Klotho-deficient mice exhibit complex ageing-like phenotypes including hypogonadism, arteriosclerosis (vascular calcification), cardiac hypertrophy, osteopenia, sarcopenia, frailty, and premature death. Klotho protein functions as the obligate co-receptor for fibroblast growth factor-23 (FGF23), a bone-derived hormone that promotes urinary phosphate excretion in response to phosphate intake. Thus, Klotho-deficient mice suffer not only from accelerated ageing but also from phosphate retention due to impaired phosphate excretion. Importantly, restoration of the phosphate balance by placing Klotho-deficient mice on low phosphate diet rescued them from premature ageing, leading us to the notion that phosphate accelerates ageing. Because the extracellular fluid is super-saturated in terms of phosphate and calcium ions, an increase in the phosphate concentration can trigger precipitation of calcium-phosphate. In the blood, calcium-phosphate precipitated upon increase in the blood phosphate concentration is adsorbed by serum protein fetuin-A to form colloidal nanoparticles called calciprotein particles (CPPs). In the urine, CPPs appear in the renal tubular fluid when FGF23 increases phosphate load excreted per nephron. CPPs can induce cell damage, ectopic calcification, and inflammatory responses. CPPs in the blood can induce arteriosclerosis and non-infectious chronic inflammation, whereas CPPs in the urine can induce renal tubular damage and interstitial inflammation/fibrosis. Thus, we propose that CPPs behave like a pathogen that accelerates ageing and should be regarded as a novel therapeutic target against age-related disorders including chronic kidney disease.
    MeSH term(s) Age Factors ; Aging/metabolism ; Aging/pathology ; Animals ; Calcium Phosphates/metabolism ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Cardiovascular Diseases/physiopathology ; Fibroblast Growth Factor-23/metabolism ; Humans ; Kidney/metabolism ; Kidney/pathology ; Kidney/physiopathology ; Klotho Proteins/metabolism ; Nanoparticles ; Phosphorus/metabolism ; Renal Elimination ; Renal Insufficiency, Chronic/metabolism ; Renal Insufficiency, Chronic/pathology ; Renal Insufficiency, Chronic/physiopathology ; alpha-2-HS-Glycoprotein/metabolism
    Chemical Substances Calcium Phosphates ; alpha-2-HS-Glycoprotein ; Phosphorus (27YLU75U4W) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; calcium phosphate (97Z1WI3NDX) ; Klotho Proteins (EC 3.2.1.31)
    Language English
    Publishing date 2021-08-10
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20201453
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Ageing-related receptors resolved.

    Kuro-O, Makoto

    Nature

    2020  Volume 553, Issue 7689, Page(s) 409–410

    Language English
    Publishing date 2020-02-20
    Publishing country England
    Document type News
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-017-09032-4
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  6. Article ; Online: Quantification of Calciprotein Particles (CPPs) in Serum/Plasma Samples Using a Fluorescent Bisphosphonate.

    Miura, Yutaka / Kurosu, Hiroshi / Kuro-O, Makoto

    Methods in molecular biology (Clifton, N.J.)

    2023  Volume 2664, Page(s) 333–341

    Abstract: Calciprotein particles (CPPs) are mineral-protein complexes containing solid-phase calcium-phosphate and the serum protein fetuin-A. CPPs are dispersed in the blood as colloids. Previous clinical studies revealed that circulating levels of CPPs were ... ...

    Abstract Calciprotein particles (CPPs) are mineral-protein complexes containing solid-phase calcium-phosphate and the serum protein fetuin-A. CPPs are dispersed in the blood as colloids. Previous clinical studies revealed that circulating levels of CPPs were correlated with inflammation and vascular calcification/stiffness in patients with chronic kidney disease (CKD). Measurement of blood CPP levels is challenging because CPPs are unstable and change their physical and chemical properties spontaneously over time in vitro. Several different methods have been developed for quantification of blood CPP levels with different advantages and limitations. We have developed a simple and sensitive assay using a fluorescent probe that bound to calcium-phosphate crystals. This assay may be useful as a clinical test to evaluate the cardiovascular risk and prognosis in CKD patients.
    MeSH term(s) Humans ; Calcium/metabolism ; Renal Insufficiency, Chronic ; Vascular Calcification ; Blood Proteins/metabolism ; Minerals ; alpha-2-HS-Glycoprotein/metabolism
    Chemical Substances Calcium (SY7Q814VUP) ; Blood Proteins ; Minerals ; alpha-2-HS-Glycoprotein
    Language English
    Publishing date 2023-07-10
    Publishing country United States
    Document type Journal Article
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-3179-9_21
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Phosphate as a Pathogen of Arteriosclerosis and Aging.

    Kuro-O, Makoto

    Journal of atherosclerosis and thrombosis

    2020  Volume 28, Issue 3, Page(s) 203–213

    Abstract: During the evolution of skeletons, terrestrial vertebrates acquired strong bones made of calcium-phosphate. By keeping the extracellular fluid in a supersaturated condition regarding calcium and phosphate ions, they created the bone when and where they ... ...

    Abstract During the evolution of skeletons, terrestrial vertebrates acquired strong bones made of calcium-phosphate. By keeping the extracellular fluid in a supersaturated condition regarding calcium and phosphate ions, they created the bone when and where they wanted simply by providing a cue for precipitation. To secure this strategy, they acquired a novel endocrine system to strictly control the extracellular phosphate concentration. In response to phosphate intake, fibroblast growth factor-23 (FGF23) is secreted from the bone and acts on the kidney through binding to its receptor Klotho to increase urinary phosphate excretion, thereby maintaining phosphate homeostasis. The FGF23-Klotho endocrine system, when disrupted in mice, results in hyperphosphatemia and vascular calcification. Besides, mice lacking Klotho or FGF23 suffer from complex aging-like phenotypes, which are alleviated by placing them on a low- phosphate diet, indicating that phosphate is primarily responsible for the accelerated aging. Phosphate acquires the ability to induce cell damage and inflammation when precipitated with calcium. In the blood, calcium-phosphate crystals are adsorbed by serum protein fetuin-A and prevented from growing into large precipitates. Consequently, nanoparticles that comprised calcium-phosphate crystals and fetuin-A, termed calciprotein particles (CPPs), are generated and dispersed as colloids. CPPs increase in the blood with an increase in serum phosphate and age. Circulating CPP levels correlate positively with vascular stiffness and chronic non-infectious inflammation, raising the possibility that CPPs may be an endogenous pro-aging factor. Terrestrial vertebrates with the bone made of calcium- phosphate may be destined to age due to calcium-phosphate in the blood.
    MeSH term(s) Aging/physiology ; Animals ; Arteriosclerosis/etiology ; Arteriosclerosis/metabolism ; Arteriosclerosis/pathology ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/physiology ; Glucuronidase/physiology ; Humans ; Klotho Proteins ; Mice ; Phosphates/physiology
    Chemical Substances FGF23 protein, human ; Fgf23 protein, mouse ; Phosphates ; Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31)
    Language English
    Publishing date 2020-10-08
    Publishing country Japan
    Document type Journal Article ; Review
    ZDB-ID 2011474-6
    ISSN 1880-3873 ; 1340-3478
    ISSN (online) 1880-3873
    ISSN 1340-3478
    DOI 10.5551/jat.RV17045
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: [Mineral metabolism and aging.]

    Kuro-O, Makoto

    Clinical calcium

    2019  Volume 29, Issue 2, Page(s) 165–170

    Abstract: Analysis of a mutant mouse exhibiting accelerated aging identified phosphorus as a pro-aging factor in mammals. In the blood, phosphorus exists in the form of phosphate ions and colloidal particles composed of solid-phase calcium-phosphate and serum ... ...

    Abstract Analysis of a mutant mouse exhibiting accelerated aging identified phosphorus as a pro-aging factor in mammals. In the blood, phosphorus exists in the form of phosphate ions and colloidal particles composed of solid-phase calcium-phosphate and serum protein fetuin-A, which are termed calciprotein particles(CPP). Blood CPP levels increase with age and decline of renal function. Because CPP have the ability to induce inflammation and vascular smooth muscle cell calcification in vitro, we hypothesize that CPP may serve as a pathogen that accelerates aging. Therapeutic interventions in phosphate and/or CPP may open a new avenue for practical anti-aging medicine.
    MeSH term(s) Animals ; Calcinosis/metabolism ; Inflammation ; Mice ; Minerals/chemistry ; Minerals/metabolism ; Myocytes, Smooth Muscle/cytology ; Myocytes, Smooth Muscle/physiology ; alpha-2-HS-Glycoprotein
    Chemical Substances Minerals ; alpha-2-HS-Glycoprotein
    Language Japanese
    Publishing date 2019-01-24
    Publishing country Japan
    Document type Journal Article
    ZDB-ID 2386417-5
    ISSN 0917-5857
    ISSN 0917-5857
    DOI 10.20837/4201902165
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  9. Article ; Online: Ageing-related receptors resolved.

    Kuro-O, Makoto

    Nature

    2018  Volume 553, Issue 7689, Page(s) 409–410

    MeSH term(s) Aging ; Humans
    Language English
    Publishing date 2018--25
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/d41586-017-09032-4
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  10. Article: Molecular Mechanisms Underlying Accelerated Aging by Defects in the FGF23-Klotho System.

    Kuro-O, Makoto

    International journal of nephrology

    2018  Volume 2018, Page(s) 9679841

    Abstract: The basic research of aging has been primarily focused on elucidating mechanisms of aging and longevity that are evolutionarily conserved from yeasts to primates. Such efforts have culminated in the notion that (1) senescence at the cellular level is ... ...

    Abstract The basic research of aging has been primarily focused on elucidating mechanisms of aging and longevity that are evolutionarily conserved from yeasts to primates. Such efforts have culminated in the notion that (1) senescence at the cellular level is associated with aging at the organismal level and that (2) calorie restriction and growth suppression decelerate aging. However, these important findings in the basic research have not necessarily been linked to improvement of daily medical practice in the aging society. It has become increasingly important to investigate mechanisms of aging unique to mammals or humans and apply the research fruits for the treatment of major age-related disorders to extend the health span. Seminal studies on the
    Language English
    Publishing date 2018-05-21
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2573904-9
    ISSN 2090-2158 ; 2090-214X
    ISSN (online) 2090-2158
    ISSN 2090-214X
    DOI 10.1155/2018/9679841
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