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Article ; Online: The Role of Zinc in Cardiovascular Disease.

Begum, Farhana / Me, Hay Me / Christov, Marta

2022 Volume 30, Issue 2, Page(s) 100–108

Abstract: Zinc is an essential trace element due to its role as a key part of human enzymatic activity. As a cofactor in metalloenzymes and metalloproteins, zinc participates in diverse biological functions, including gene transcription, translation, and ... ...

Abstract	Zinc is an essential trace element due to its role as a key part of human enzymatic activity. As a cofactor in metalloenzymes and metalloproteins, zinc participates in diverse biological functions, including gene transcription, translation, and replication, phagocytosis, and immunoglobulin and cytokine production. In this review, we will focus on the role of zinc in the cardiovascular system, including heart failure, vascular calcification, and myocardial infarction. We will further highlight the role of zinc in cardiovascular pathology in individuals with chronic kidney disease, and type II diabetes mellitus, groups uniquely at risk for cardiovascular morbidity and mortality.
MeSH term(s)	Cardiovascular Diseases ; Diabetes Mellitus, Type 2 ; Humans ; Metalloproteins ; Renal Insufficiency, Chronic ; Zinc
Chemical Substances	Metalloproteins ; Zinc (J41CSQ7QDS)
Language	English
Publishing date	2022-02-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1294965-6
ISSN	1538-4683 ; 1061-5377
ISSN (online)	1538-4683
ISSN	1061-5377
DOI	10.1097/CRD.0000000000000382
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Article ; Online: Fibroblast growth factor 23 in acute kidney injury.

Christov, Marta

Current opinion in nephrology and hypertension

2014 Volume 23, Issue 4, Page(s) 340–345

Abstract: Purpose of review: To review the emerging literature on changes in fibroblast growth factor 23 (FGF23) levels in the setting of acute kidney injury (AKI).: Recent findings: Studies suggest that FGF23 levels are elevated in patients with AKI and ... ...

Abstract	Purpose of review: To review the emerging literature on changes in fibroblast growth factor 23 (FGF23) levels in the setting of acute kidney injury (AKI). Recent findings: Studies suggest that FGF23 levels are elevated in patients with AKI and correlate with increased risk of death or need for dialysis in adults, or prolonged ventilation time and higher fluid gain in children. Animal studies have shown that the cause behind this FGF23 increase is multifactorial and includes increased production in bone and decreased clearance, but not vitamin D or parathyroid hormone (PTH) activated pathways. Interestingly, FGF23 levels are found to be mildly elevated even in hospitalized patients without kidney injury, although this observation may be limited to only c-terminal FGF23 fragments. The prognostic implications of an elevated FGF23 value in patients with AKI need to be confirmed in larger cohorts and evaluated for long-term outcomes such as the development of new chronic kidney disease (CKD) or CKD progression, as well as cardiovascular disease, similar to the studies of FGF23 in the prevalent CKD population. Summary: FGF23 levels are elevated in patients with AKI and are associated with morbidity and mortality in small human studies. Mechanistic work in animals suggests that the elevation is independent of PTH or vitamin D signaling pathways. Much work remains to understand the physiology behind FGF23 elevation and the long-term effects of FGF23 in AKI.
MeSH term(s)	Acute Kidney Injury/metabolism ; Animals ; Calcitriol/metabolism ; Fibroblast Growth Factors/blood ; Humans ; Parathyroid Hormone/metabolism ; Phosphates/metabolism ; Renal Insufficiency, Chronic/metabolism ; Signal Transduction
Chemical Substances	Parathyroid Hormone ; Phosphates ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE) ; Calcitriol (FXC9231JVH)
Language	English
Publishing date	2014-05-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
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	10.1097/01.mnh.0000447021.51722.2f
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Zs.A 3686: Show issues

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Article ; Online: Dysregulated Mineral Metabolism in AKI.

Leaf, David E / Christov, Marta

Seminars in nephrology

2019 Volume 39, Issue 1, Page(s) 41–56

Abstract: Dysregulated mineral metabolism is a nearly universal sequalae of acute kidney injury (AKI). Abnormalities in circulating mineral metabolites observed in patients with AKI include hypocalcemia, hyperparathyroidism, hyperphosphatemia, decreased vitamin D ... ...

Abstract	Dysregulated mineral metabolism is a nearly universal sequalae of acute kidney injury (AKI). Abnormalities in circulating mineral metabolites observed in patients with AKI include hypocalcemia, hyperparathyroidism, hyperphosphatemia, decreased vitamin D metabolite levels, and increased fibroblast growth factor 23 levels. We review the pathophysiology of dysregulated mineral metabolism in AKI with a focus on calcium, phosphate, parathyroid hormone, and vitamin D metabolites. We discuss how mineral metabolite levels can serve as novel prognostic markers for incident AKI and other related outcomes in various clinical settings. Finally, we discuss how vitamin D metabolites potentially could be used as novel therapeutic agents for AKI prevention and treatment.
MeSH term(s)	Acute Kidney Injury/complications ; Acute Kidney Injury/physiopathology ; Acute Kidney Injury/therapy ; Animals ; Fibroblast Growth Factors/metabolism ; Humans ; Hyperparathyroidism/blood ; Hyperparathyroidism/etiology ; Hyperphosphatemia/etiology ; Hyperphosphatemia/therapy ; Hypocalcemia/etiology ; Hypocalcemia/physiopathology ; Membrane Proteins/metabolism ; Minerals/metabolism ; Parathyroid Hormone/blood ; Renal Replacement Therapy/adverse effects ; Vitamin D/analogs & derivatives ; Vitamin D/blood ; Vitamin D/therapeutic use ; Vitamin D Deficiency/blood ; Vitamin D Deficiency/drug therapy ; Vitamin D Deficiency/etiology
Chemical Substances	KLB protein, human ; Membrane Proteins ; Minerals ; Parathyroid Hormone ; Vitamin D (1406-16-2) ; Fibroblast Growth Factors (62031-54-3) ; 1,25-dihydroxyvitamin D (66772-14-3) ; fibroblast growth factor 23 (7Q7P4S7RRE) ; 25-hydroxyvitamin D (A288AR3C9H)
Language	English
Publishing date	2019-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2018.10.004
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Article ; Online: Phosphate homeostasis disorders.

Christov, Marta / Jüppner, Harald

Best practice & research. Clinical endocrinology & metabolism

2018 Volume 32, Issue 5, Page(s) 685–706

Abstract: Our understanding of the regulation of phosphate balance has benefited tremendously from the molecular identification and characterization of genetic defects leading to a number of rare inherited or acquired disorders affecting phosphate homeostasis. The ...

Abstract	Our understanding of the regulation of phosphate balance has benefited tremendously from the molecular identification and characterization of genetic defects leading to a number of rare inherited or acquired disorders affecting phosphate homeostasis. The identification of the key phosphate-regulating hormone, fibroblast growth factor 23 (FGF23), as well as other molecules that control its production, such as the glycosyltransferase GALNT3, the endopeptidase PHEX, and the matrix protein DMP1, and molecules that function as downstream effectors of FGF23 such as the longevity factor Klotho and the phosphate transporters NPT2a and NPT2c, has permitted us to understand the complex interplay that exists between the kidneys, bone, parathyroid, and gut. Such insights from genetic disorders have allowed not only the design of potent targeted treatment of FGF23-dependent hypophosphatemic conditions, but also provide clinically relevant observations related to the dysregulation of mineral ion homeostasis in health and disease.
MeSH term(s)	Bone and Bones/metabolism ; Fibroblast Growth Factors/physiology ; Homeostasis/physiology ; Humans ; Hypophosphatemia/genetics ; Hypophosphatemia/metabolism ; Kidney/metabolism ; Metabolic Networks and Pathways/genetics ; Phosphates/metabolism ; Phosphorus Metabolism Disorders/diagnosis ; Phosphorus Metabolism Disorders/genetics ; Phosphorus Metabolism Disorders/metabolism
Chemical Substances	Phosphates ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE)
Language	English
Publishing date	2018-06-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2052339-7
ISSN	1878-1594 ; 1532-1908 ; 1521-690X
ISSN (online)	1878-1594 ; 1532-1908
ISSN	1521-690X
DOI	10.1016/j.beem.2018.06.004
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Article ; Online: Clearance of FGF-23 during continuous renal replacement therapy.

Sharma, Shilpa / Christov, Marta / Ix, Joachim H / Waikar, Sushrut S

Hemodialysis international. International Symposium on Home Hemodialysis

2019 Volume 23, Issue 3, Page(s) 366–368

Abstract: FGF-23 is a 32 kDa protein that is a key regulator of phosphorus and vitamin D metabolism. Emerging evidence also demonstrates that FGF-23 increases within 24 hours of acute kidney injury (AKI) and may be associated with adverse clinical outcomes. We ... ...

Abstract	FGF-23 is a 32 kDa protein that is a key regulator of phosphorus and vitamin D metabolism. Emerging evidence also demonstrates that FGF-23 increases within 24 hours of acute kidney injury (AKI) and may be associated with adverse clinical outcomes. We conducted this study to evaluate FGF23 clearance during continuous veno-venous hemofiltration (CVVH) in critically ill patients with AKI. We demonstrate that plasma clearance of FGF-23 during CVVH is ∼11 mL/min and the mean sieving coefficient is 0.27 ± 0.1. Future studies will need to clarify FGF-23's role in adverse outcomes among AKI patients, and whether therapies aimed at reducing FGF-23 levels may be beneficial.
MeSH term(s)	Continuous Renal Replacement Therapy/methods ; Female ; Fibroblast Growth Factors/pharmacology ; Fibroblast Growth Factors/therapeutic use ; Hemofiltration/methods ; Humans ; Male ; Middle Aged
Chemical Substances	Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE)
Language	English
Publishing date	2019-04-30
Publishing country	Canada
Document type	Letter ; Research Support, N.I.H., Extramural
ZDB-ID	2192458-2
ISSN	1542-4758 ; 1492-7535
ISSN (online)	1542-4758
ISSN	1492-7535
DOI	10.1111/hdi.12758
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Article ; Online: Fibroblast Growth Factor 23 and Klotho in AKI.

Christov, Marta / Neyra, Javier A / Gupta, Sanjeev / Leaf, David E

Seminars in nephrology

2019 Volume 39, Issue 1, Page(s) 57–75

Abstract: Acute kidney injury (AKI) is associated with many of the same mineral metabolite abnormalities that are observed in chronic kidney disease. These include increased circulating levels of the osteocyte-derived, vitamin D-regulating hormone, fibroblast ... ...

Abstract	Acute kidney injury (AKI) is associated with many of the same mineral metabolite abnormalities that are observed in chronic kidney disease. These include increased circulating levels of the osteocyte-derived, vitamin D-regulating hormone, fibroblast growth factor 23 (FGF23), and decreased renal expression of klotho, the co-receptor for FGF23. Recent data have indicated that increased FGF23 and decreased klotho levels in the blood and urine could serve as novel predictive biomarkers of incident AKI, or as novel prognostic biomarkers of adverse outcomes in patients with established AKI. In addition, because FGF23 and klotho exert numerous classic as well as off-target effects on a variety of organ systems, targeting their dysregulation in AKI may represent a unique opportunity for therapeutic intervention. We review the pathophysiology, kinetics, and regulation of FGF23 and klotho in animal and human studies of AKI, and we discuss the challenges and opportunities involved in targeting FGF23 and klotho therapeutically.
MeSH term(s)	Acute Kidney Injury/blood ; Acute Kidney Injury/etiology ; Acute Kidney Injury/therapy ; Animals ; Biomarkers/blood ; Cardiac Surgical Procedures/adverse effects ; Critical Illness ; Fibroblast Growth Factors/antagonists & inhibitors ; Fibroblast Growth Factors/blood ; Fibroblast Growth Factors/metabolism ; Fibroblast Growth Factors/physiology ; Fibrosis ; Glucuronidase/genetics ; Glucuronidase/metabolism ; Glucuronidase/physiology ; Glucuronidase/therapeutic use ; Humans ; Kidney/pathology ; Prognosis ; Renal Insufficiency, Chronic/blood ; Severity of Illness Index ; Signal Transduction
Chemical Substances	Biomarkers ; Fgf23 protein, rat ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE) ; Glucuronidase (EC 3.2.1.31) ; klotho protein (EC 3.2.1.31)
Language	English
Publishing date	2019-01-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2018.10.005
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Article ; Online: Screen for Small-Molecule Modulators of Circadian Rhythms Reveals Phenazine as a Redox-State Modifying Clockwork Tuner.

Kelly, Kevin P / Borsetti, Hugo / Wenzler, Marta E / Ustione, Alessandro / Kim, Kwangho / Christov, Plamen P / Ramirez, Bianca / Bauer, Joshua A / Piston, David W / Johnson, Carl Hirschie / Sulikowski, Gary A

ACS chemical biology

2022 Volume 17, Issue 7, Page(s) 1658–1664

Abstract: A high-throughput cell-based screen identified redox-active small molecules that produce a period lengthening of the circadian rhythm. The strongest period lengthening phenotype was induced by a phenazine carboxamide (VU661). Comparison to two isomeric ... ...

Abstract	A high-throughput cell-based screen identified redox-active small molecules that produce a period lengthening of the circadian rhythm. The strongest period lengthening phenotype was induced by a phenazine carboxamide (VU661). Comparison to two isomeric benzquinoline carboxamides (VU673 and VU164) shows the activity is associated with the redox modulating phenazine functionality. Furthermore, ex vivo cell analysis using optical redox ratio measurements shows the period lengthening phenotype to be associated with a shift to the NAD/FAD oxidation state of nicotinamide and flavine coenzymes.
MeSH term(s)	Circadian Rhythm ; Oxidation-Reduction ; Phenazines
Chemical Substances	Phenazines
Language	English
Publishing date	2022-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	1554-8937
ISSN (online)	1554-8937
DOI	10.1021/acschembio.2c00240
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Article ; Online: Dietary phosphate: the challenges of exploring its role in FGF23 regulation.

Christov, Marta / Jüppner, Harald

Kidney international

2013 Volume 84, Issue 4, Page(s) 639–641

Abstract: Fibroblast growth factor 23 (FGF23) is an important regulator of phosphate homeostasis, yet efforts to control its circulating levels by manipulating dietary phosphate intake in humans and animals with normal or impaired kidney function have yielded ... ...

Abstract	Fibroblast growth factor 23 (FGF23) is an important regulator of phosphate homeostasis, yet efforts to control its circulating levels by manipulating dietary phosphate intake in humans and animals with normal or impaired kidney function have yielded conflicting results. In the study by Zhang et al., severe phosphate restriction in a genetic mouse model of progressive kidney dysfunction failed to cause a uniform FGF23 reduction, again highlighting the complexity of FGF23 regulation.
MeSH term(s)	Acute Kidney Injury/blood ; Acute Kidney Injury/physiopathology ; Animals ; Female ; Fibroblast Growth Factors/blood ; Fibroblast Growth Factors/metabolism ; Humans ; Hypophosphatemia, Familial/metabolism ; Hypophosphatemia, Familial/prevention & control ; Male ; Nephritis, Hereditary/metabolism ; Phosphates/administration & dosage ; Phosphates/deficiency ; Renal Insufficiency, Chronic/metabolism ; Signal Transduction/physiology
Chemical Substances	Phosphates ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE)
Language	English
Publishing date	2013-10-01
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1038/ki.2013.198
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Zs.A 797: Show issues

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Article ; Online: Insights from genetic disorders of phosphate homeostasis.

Christov, Marta / Jüppner, Harald

Seminars in nephrology

2013 Volume 33, Issue 2, Page(s) 143–157

Abstract: The molecular identification and characterization of genetic defects leading to a number of rare inherited or acquired disorders affecting phosphate homeostasis has added tremendous detail to our understanding of the regulation of phosphate balance. The ... ...

Abstract	The molecular identification and characterization of genetic defects leading to a number of rare inherited or acquired disorders affecting phosphate homeostasis has added tremendous detail to our understanding of the regulation of phosphate balance. The identification of the key phosphate-regulating hormone, fibroblast growth factor 23 (FGF23), as well as other molecules that control its production, such as the N-acetylgalactosaminyltransferase 3 GALNT3, the endopeptidase phosphate-regulating protein with homologies to endopeptidases on the X chromosome, and the matrix protein dentin matrix protein 1, and molecules that function as downstream effectors of FGF23, such as the longevity factor Klotho and the phosphate transporters NPT2a and NPT2c, has permitted us to understand the elegant and complex interplay that exists between the kidneys, bone, parathyroid, and gut. Such insights from genetic disorders have allowed not only the design of potent targeted therapies for some of these rare genetic disorders, such as using anti-FGF23 antibodies for treatment of X-linked hypophosphatemic rickets, but also have led to clinically relevant observations related to the dysregulation of mineral ion homeostasis in chronic kidney disease. Thus, we are able to leverage our knowledge of rare human disorders affecting only a few individuals, to understand and potentially treat disease processes that affect millions of patients.
MeSH term(s)	Fibroblast Growth Factors/physiology ; Homeostasis ; Humans ; Phosphates/metabolism ; Phosphorus Metabolism Disorders/genetics ; Renal Insufficiency, Chronic/metabolism
Chemical Substances	Phosphates ; Fibroblast Growth Factors (62031-54-3) ; fibroblast growth factor 23 (7Q7P4S7RRE)
Language	English
Publishing date	2013-03-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	604652-6
ISSN	1558-4488 ; 0270-9295
ISSN (online)	1558-4488
ISSN	0270-9295
DOI	10.1016/j.semnephrol.2012.12.015
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Article ; Online: Tubular transport: core curriculum 2010.

Christov, Marta / Alper, Seth L

American journal of kidney diseases : the official journal of the National Kidney Foundation

2010 Volume 56, Issue 6, Page(s) 1202–1217

MeSH term(s)	Biological Transport/physiology ; Cell Polarity/physiology ; Humans ; Kidney Tubules/cytology ; Kidney Tubules/physiology ; Podocytes/physiology
Language	English
Publishing date	2010-10-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	604539-x
ISSN	1523-6838 ; 0272-6386
ISSN (online)	1523-6838
ISSN	0272-6386
DOI	10.1053/j.ajkd.2010.09.011
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