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Article ; Online: Erythroferrone in iron regulation and beyond.

Babitt, Jodie L

2022 Volume 139, Issue 3, Page(s) 319–321

MeSH term(s)	Erythropoiesis ; Hepcidins ; Iron
Chemical Substances	Hepcidins ; Iron (E1UOL152H7)
Language	English
Publishing date	2022-01-20
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2021014326
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Article ; Online: Ironing out pulmonary arterial hypertension.

Babitt, Jodie L

Proceedings of the National Academy of Sciences of the United States of America

2019 Volume 116, Issue 26, Page(s) 12604–12606

MeSH term(s)	Anemia, Iron-Deficiency ; Animals ; Hypertension, Pulmonary ; Mice ; Myocytes, Smooth Muscle ; Pulmonary Arterial Hypertension ; Pulmonary Artery
Language	English
Publishing date	2019-06-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1908298116
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Article ; Online: Pumping iron in the kidney.

Fisher, Allison L / Babitt, Jodie L

Kidney international

2021 Volume 100, Issue 3, Page(s) 505–508

Abstract: Iron balance is tightly controlled to provide adequate amounts of this essential nutrient, but to limit the adverse effects of excess iron. Key mediators of systemic iron homeostasis are the iron regulatory hormone hepcidin and its receptor, the iron ... ...

Abstract	Iron balance is tightly controlled to provide adequate amounts of this essential nutrient, but to limit the adverse effects of excess iron. Key mediators of systemic iron homeostasis are the iron regulatory hormone hepcidin and its receptor, the iron export protein ferroportin. A new study by Mohammad et al. demonstrates the functional role of the hepcidin-ferroportin axis in the kidney, and how this contributes to kidney iron levels and the systemic iron economy.
MeSH term(s)	Homeostasis ; Humans ; Iron ; Iron Overload/drug therapy ; Kidney
Chemical Substances	Iron (E1UOL152H7)
Language	English
Publishing date	2021-08-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2021.06.023
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Zs.A 797: Show issues

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Article ; Online: Coordination of iron homeostasis by bone morphogenetic proteins: Current understanding and unanswered questions.

Fisher, Allison L / Babitt, Jodie L

Developmental dynamics : an official publication of the American Association of Anatomists

2021 Volume 251, Issue 1, Page(s) 26–46

Abstract: Iron homeostasis is tightly regulated to balance the iron requirement for erythropoiesis and other vital cellular functions, while preventing cellular injury from iron excess. The liver hormone hepcidin is the master regulator of systemic iron balance by ...

Abstract	Iron homeostasis is tightly regulated to balance the iron requirement for erythropoiesis and other vital cellular functions, while preventing cellular injury from iron excess. The liver hormone hepcidin is the master regulator of systemic iron balance by controlling the degradation and function of the sole known mammalian iron exporter ferroportin. Liver hepcidin expression is coordinately regulated by several signals that indicate the need for more or less iron, including plasma and tissue iron levels, inflammation, and erythropoietic drive. Most of these signals regulate hepcidin expression by modulating the activity of the bone morphogenetic protein (BMP)-SMAD pathway, which controls hepcidin transcription. Genetic disorders of iron overload and iron deficiency have identified several hepatocyte membrane proteins that play a critical role in mediating the BMP-SMAD and hepcidin regulatory response to iron. However, the precise molecular mechanisms by which serum and tissue iron levels are sensed to regulate BMP ligand production and promote the physical and/or functional interaction of these proteins to modulate SMAD signaling and hepcidin expression remain uncertain. This critical commentary will focus on the current understanding and key unanswered questions regarding how the liver senses iron levels to regulate BMP-SMAD signaling and thereby hepcidin expression to control systemic iron homeostasis.
MeSH term(s)	Animals ; Bone Morphogenetic Proteins/metabolism ; Hepatocytes/metabolism ; Homeostasis ; Iron/metabolism ; Iron Overload/genetics ; Iron Overload/metabolism ; Mammals/metabolism
Chemical Substances	Bone Morphogenetic Proteins ; Iron (E1UOL152H7)
Language	English
Publishing date	2021-05-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1102541-4
ISSN	1097-0177 ; 1058-8388
ISSN (online)	1097-0177
ISSN	1058-8388
DOI	10.1002/dvdy.372
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Article ; Online: Regulation of FGF23: Beyond Bone.

Simic, Petra / Babitt, Jodie L

Current osteoporosis reports

2021 Volume 19, Issue 6, Page(s) 563–573

Abstract: Purpose of review: Fibroblast growth factor 23 (FGF23) is a bone- and bone marrow-derived hormone that is critical to maintain phosphate homeostasis. The principal actions of FGF23 are to reduce serum phosphate levels by decreasing kidney phosphate ... ...

Abstract	Purpose of review: Fibroblast growth factor 23 (FGF23) is a bone- and bone marrow-derived hormone that is critical to maintain phosphate homeostasis. The principal actions of FGF23 are to reduce serum phosphate levels by decreasing kidney phosphate reabsorption and 1,25-dihydroxyvitamin D synthesis. FGF23 deficiency causes hyperphosphatemia and ectopic calcifications, while FGF23 excess causes hypophosphatemia and skeletal defects. Excess FGF23 also correlates with kidney disease, where it is associated with increased morbidity and mortality. Accordingly, FGF23 levels are tightly regulated, but the mechanisms remain incompletely understood. Recent findings: In addition to bone mineral factors, additional factors including iron, erythropoietin, inflammation, energy, and metabolism regulate FGF23. All these factors affect Fgf23 expression, while some also regulate FGF23 protein cleavage. Conversely, FGF23 may have a functional role in regulating these biologic processes. Understanding the bi-directional relationship between FGF23 and non-bone mineral factors is providing new insights into FGF23 regulation and function.
MeSH term(s)	Animals ; Bone and Bones/metabolism ; Energy Metabolism ; Erythropoiesis ; Fibroblast Growth Factor-23/metabolism ; Homeostasis ; Humans ; Inflammation/metabolism ; Iron Deficiencies/metabolism ; Mice
Chemical Substances	FGF23 protein, human ; Fibroblast Growth Factor-23 (7Q7P4S7RRE)
Language	English
Publishing date	2021-11-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2186581-4
ISSN	1544-2241 ; 1544-1873
ISSN (online)	1544-2241
ISSN	1544-1873
DOI	10.1007/s11914-021-00703-w
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Article ; Online: Glycerol-3-phosphate and fibroblast growth factor 23 regulation.

Simic, Petra / Babitt, Jodie L / Rhee, Eugene P

Current opinion in nephrology and hypertension

2021 Volume 30, Issue 4, Page(s) 397–403

Abstract: Purpose of review: Both classical and nonclassical factors regulate fibroblast growth factor 23 (FGF23), with impacts on gene expression and proteolytic cleavage. Here, we review recent publications that extend current knowledge on these factors.: ... ...

Abstract	Purpose of review: Both classical and nonclassical factors regulate fibroblast growth factor 23 (FGF23), with impacts on gene expression and proteolytic cleavage. Here, we review recent publications that extend current knowledge on these factors. Recent findings: Emerging nonclassical FGF23 regulators such as erythropoietin cause a balanced increase in FGF23 expression and cleavage, with minimal or no increase in biologically active intact FGF23 (iFGF23) in blood. However, circulating FGF23 profiles may not reflect the bone marrow microenvironment. For example, granulocyte colony-stimulating factor increases local marrow iFGF23 levels without impacting circulating iFGF23 levels. The view that phosphate does not increase bone FGF23 production also warrants reconsideration, as phosphate can reduce iFGF23 cleavage and phosphate-containing calciprotein particles increase FGF23 expression. Finally, a screen of renal venous plasma identifies glycerol-3-phosphate as a kidney-derived molecule that circulates to bone and bone marrow, where it is converted to lysophosphatidic acid and signals through a G-protein coupled receptor to increase FGF23 synthesis. Summary: FGF23 regulation is complex, requiring consideration of known and emerging stimuli, expression and cleavage, and circulating and local levels. Recent work identifies glycerol-3-phosphate as an FGF23 regulator derived from the injured kidney; whether it participates in FGF23 production downstream of classical or nonclassical factors requires further study.
MeSH term(s)	Fibroblast Growth Factor-23 ; Fibroblast Growth Factors ; Glycerol ; Humans ; Kidney ; Phosphates
Chemical Substances	FGF23 protein, human ; Phosphates ; Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Glycerol (PDC6A3C0OX)
Language	English
Publishing date	2021-04-28
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/MNH.0000000000000715
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Zs.A 3686: Show issues

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Article ; Online: Crosstalk between fibroblast growth factor 23, iron, erythropoietin, and inflammation in kidney disease.

Babitt, Jodie L / Sitara, Despina

Current opinion in nephrology and hypertension

2019 Volume 28, Issue 4, Page(s) 304–310

Abstract: Purpose of review: Recent research has revealed that regulation of the bone-secreted hormone fibroblast growth factor 23 (FGF23) is not limited to classical mineral factors. Specifically, bidirectional relationships have been described between FGF23 ... ...

Abstract	Purpose of review: Recent research has revealed that regulation of the bone-secreted hormone fibroblast growth factor 23 (FGF23) is not limited to classical mineral factors. Specifically, bidirectional relationships have been described between FGF23 production and anemia, iron status, and inflammation. Here, we will review the latest published articles on the crosstalk between FGF23 and the aforementioned nonclassical factors. Recent findings: It has been recently reported that erythropoietin, iron deficiency, and inflammation increase FGF23 production and metabolism. Moreover, FGF23 promotes anemia and regulates inflammatory responses. These findings are particularly important in the setting of chronic kidney disease which is characterized by elevated FGF23 levels and several associated comorbidities. Summary: Regulation of FGF23 is complex and involves many bone and renal factors. More recently, erythropoietin, iron deficiency, and inflammation have been also shown to affect FGF23 transcription and cleavage. Importantly, FGF23 has emerged as a regulator of erythropoiesis, iron metabolism, and inflammation. These findings provide novel and important insights into the pathophysiologic mechanisms of chronic kidney disease and may present new opportunities for therapeutic clinical interventions.
MeSH term(s)	Erythropoiesis ; Erythropoietin/physiology ; Fibroblast Growth Factor-23 ; Fibroblast Growth Factors/physiology ; Humans ; Inflammation/complications ; Iron/metabolism ; Renal Insufficiency, Chronic/etiology
Chemical Substances	FGF23 protein, human ; Erythropoietin (11096-26-7) ; Fibroblast Growth Factors (62031-54-3) ; Fibroblast Growth Factor-23 (7Q7P4S7RRE) ; Iron (E1UOL152H7)
Language	English
Publishing date	2019-03-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; 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/MNH.0000000000000514
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Article ; Online: Endothelial ZIP8 plays a minor role in BMP6 regulation by iron in mice.

Fisher, Allison L / Phillips, Sydney / Wang, Chia-Yu / Paulo, Joao A / Xiao, Xia / Moschetta, Gillian A / Sridhar, Adhvaith / Mancias, Joseph D / Babitt, Jodie L

Blood

2024

Abstract: Iron-mediated induction of BMP6 expression by liver endothelial cells is essential for iron homeostasis regulation. We utilized multiple dietary and genetic mouse cohorts to demonstrate a minor functional role for ZIP8 in regulating BMP6 expression under ...

Abstract	Iron-mediated induction of BMP6 expression by liver endothelial cells is essential for iron homeostasis regulation. We utilized multiple dietary and genetic mouse cohorts to demonstrate a minor functional role for ZIP8 in regulating BMP6 expression under high-iron conditions.
Language	English
Publishing date	2024-03-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2023023385
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Article ; Online: Liver iron sensing and body iron homeostasis.

Wang, Chia-Yu / Babitt, Jodie L

Blood

2018 Volume 133, Issue 1, Page(s) 18–29

Abstract: The liver orchestrates systemic iron balance by producing and secreting hepcidin. Known as the iron hormone, hepcidin induces degradation of the iron exporter ferroportin to control iron entry into the bloodstream from dietary sources, iron recycling ... ...

Abstract	The liver orchestrates systemic iron balance by producing and secreting hepcidin. Known as the iron hormone, hepcidin induces degradation of the iron exporter ferroportin to control iron entry into the bloodstream from dietary sources, iron recycling macrophages, and body stores. Under physiologic conditions, hepcidin production is reduced by iron deficiency and erythropoietic drive to increase the iron supply when needed to support red blood cell production and other essential functions. Conversely, hepcidin production is induced by iron loading and inflammation to prevent the toxicity of iron excess and limit its availability to pathogens. The inability to appropriately regulate hepcidin production in response to these physiologic cues underlies genetic disorders of iron overload and deficiency, including hereditary hemochromatosis and iron-refractory iron deficiency anemia. Moreover, excess hepcidin suppression in the setting of ineffective erythropoiesis contributes to iron-loading anemias such as β-thalassemia, whereas excess hepcidin induction contributes to iron-restricted erythropoiesis and anemia in chronic inflammatory diseases. These diseases have provided key insights into understanding the mechanisms by which the liver senses plasma and tissue iron levels, the iron demand of erythrocyte precursors, and the presence of potential pathogens and, importantly, how these various signals are integrated to appropriately regulate hepcidin production. This review will focus on recent insights into how the liver senses body iron levels and coordinates this with other signals to regulate hepcidin production and systemic iron homeostasis.
MeSH term(s)	Homeostasis ; Humans ; Iron/metabolism ; Iron Metabolism Disorders/physiopathology ; Liver/metabolism
Chemical Substances	Iron (E1UOL152H7)
Language	English
Publishing date	2018-11-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2018-06-815894
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Article ; Online: Bone morphogenic proteins in iron homeostasis.

Xiao, Xia / Alfaro-Magallanes, Víctor M / Babitt, Jodie L

Bone

2020 Volume 138, Page(s) 115495

Abstract: The bone morphogenetic protein (BMP)-SMAD signaling pathway plays a central role in regulating hepcidin, which is the master hormone governing systemic iron homeostasis. Hepcidin is produced by the liver and acts on the iron exporter ferroportin to ... ...

Abstract	The bone morphogenetic protein (BMP)-SMAD signaling pathway plays a central role in regulating hepcidin, which is the master hormone governing systemic iron homeostasis. Hepcidin is produced by the liver and acts on the iron exporter ferroportin to control iron absorption from the diet and iron release from body stores, thereby providing adequate iron for red blood cell production, while limiting the toxic effects of excess iron. BMP6 and BMP2 ligands produced by liver endothelial cells bind to BMP receptors and the coreceptor hemojuvelin (HJV) on hepatocytes to activate SMAD1/5/8 signaling, which directly upregulates hepcidin transcription. Most major signals that influence hepcidin production, including iron, erythropoietic drive, and inflammation, intersect with the BMP-SMAD pathway to regulate hepcidin transcription. Mutation or inactivation of BMP ligands, BMP receptors, HJV, SMADs or other proteins that modulate the BMP-SMAD pathway result in hepcidin dysregulation, leading to iron-related disorders, such as hemochromatosis and iron refractory iron deficiency anemia. Pharmacologic modulators of the BMP-SMAD pathway have shown efficacy in pre-clinical models to regulate hepcidin expression and treat iron-related disorders. This review will discuss recent insights into the role of the BMP-SMAD pathway in regulating hepcidin to control systemic iron homeostasis.
MeSH term(s)	Animals ; Bone Morphogenetic Proteins ; Endothelial Cells ; GPI-Linked Proteins ; Hepatocytes ; Homeostasis ; Humans ; Iron
Chemical Substances	Bone Morphogenetic Proteins ; GPI-Linked Proteins ; Iron (E1UOL152H7)
Language	English
Publishing date	2020-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2020.115495
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