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Article ; Online: HEME: a neglected player in nociception?

Chiabrando, Deborah / Fiorito, Veronica / Petrillo, Sara / Bertino, Francesca / Tolosano, Emanuela

2021 Volume 124, Page(s) 124–136

Abstract: Despite increasing progress in the understanding of the pathophysiology of pain, current management of pain syndromes is still unsatisfactory. The recent discovery of novel pathways associated with pain insensitivity in humans represents a unique ... ...

Abstract	Despite increasing progress in the understanding of the pathophysiology of pain, current management of pain syndromes is still unsatisfactory. The recent discovery of novel pathways associated with pain insensitivity in humans represents a unique opportunity to improve our knowledge on the pathophysiology of pain. Heme metabolism recently emerged as a crucial regulator of nociception. Of note, alteration of heme metabolism has been associated with pain insensitivity as well as with acute and chronic pain in porphyric neuropathy and hemolytic diseases. However, the molecular mechanisms linking heme to the pain pathways still remain unclear. The review focuses on the major heme-regulated processes relevant for sensory neurons' maintenance, peripheral and central sensitization as well as for pain comorbidities, like anxiety and depression. By discussing the body of knowledge on the topic, we provide a novel perspective on the molecular mechanisms linking heme to nociception.
MeSH term(s)	Heme/metabolism ; Humans ; Membrane Transport Proteins ; Nociception ; Pain ; Receptors, Virus/metabolism
Chemical Substances	Membrane Transport Proteins ; Receptors, Virus ; Heme (42VZT0U6YR)
Language	English
Publishing date	2021-02-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	282464-4
ISSN	1873-7528 ; 0149-7634
ISSN (online)	1873-7528
ISSN	0149-7634
DOI	10.1016/j.neubiorev.2021.01.011
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Article ; Online: Hereditary Ataxia: A Focus on Heme Metabolism and Fe-S Cluster Biogenesis.

Chiabrando, Deborah / Bertino, Francesca / Tolosano, Emanuela

International journal of molecular sciences

2020 Volume 21, Issue 11

Abstract: Heme and Fe-S clusters regulate a plethora of essential biological processes ranging from cellular respiration and cell metabolism to the maintenance of genome integrity. Mutations in genes involved in heme metabolism and Fe-S cluster biogenesis cause ... ...

Abstract	Heme and Fe-S clusters regulate a plethora of essential biological processes ranging from cellular respiration and cell metabolism to the maintenance of genome integrity. Mutations in genes involved in heme metabolism and Fe-S cluster biogenesis cause different forms of ataxia, like posterior column ataxia and retinitis pigmentosa (PCARP), Friedreich's ataxia (FRDA) and X-linked sideroblastic anemia with ataxia (XLSA/A). Despite great efforts in the elucidation of the molecular pathogenesis of these disorders several important questions still remain to be addressed. Starting with an overview of the biology of heme metabolism and Fe-S cluster biogenesis, the review discusses recent progress in the understanding of the molecular pathogenesis of PCARP, FRDA and XLSA/A, and highlights future line of research in the field. A better comprehension of the mechanisms leading to the degeneration of neural circuity responsible for balance and coordinated movement will be crucial for the therapeutic management of these patients.
MeSH term(s)	Anemia, Sideroblastic/genetics ; Anemia, Sideroblastic/metabolism ; Animals ; Ataxia/genetics ; Ataxia/metabolism ; Friedreich Ataxia/genetics ; Friedreich Ataxia/metabolism ; Genetic Diseases, X-Linked/genetics ; Genetic Diseases, X-Linked/metabolism ; Heme/genetics ; Heme/metabolism ; Humans ; Iron-Sulfur Proteins/genetics ; Iron-Sulfur Proteins/metabolism ; Retinitis Pigmentosa/genetics ; Retinitis Pigmentosa/metabolism ; Spinocerebellar Ataxias/genetics ; Spinocerebellar Ataxias/metabolism
Chemical Substances	Iron-Sulfur Proteins ; Heme (42VZT0U6YR)
Language	English
Publishing date	2020-05-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21113760
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Article: The Multifaceted Role of Heme in Cancer.

Fiorito, Veronica / Chiabrando, Deborah / Petrillo, Sara / Bertino, Francesca / Tolosano, Emanuela

Frontiers in oncology

2020 Volume 9, Page(s) 1540

Abstract: Heme, an iron-containing porphyrin, is of vital importance for cells due to its involvement in several biological processes, including oxygen transport, energy production and drug metabolism. Besides these vital functions, heme also bears toxic ... ...

Abstract	Heme, an iron-containing porphyrin, is of vital importance for cells due to its involvement in several biological processes, including oxygen transport, energy production and drug metabolism. Besides these vital functions, heme also bears toxic properties and, therefore, the amount of heme inside the cells must be tightly regulated. Similarly, heme intake from dietary sources is strictly controlled to meet body requirements. The multifaceted nature of heme renders it a best candidate molecule exploited/controlled by tumor cells in order to modulate their energetic metabolism, to interact with the microenvironment and to sustain proliferation and survival. The present review summarizes the literature on heme and cancer, emphasizing the importance to consider heme as a prominent player in different aspects of tumor onset and progression.
Language	English
Publishing date	2020-01-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2019.01540
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Article ; Online: Hereditary Ataxia

Deborah Chiabrando / Francesca Bertino / Emanuela Tolosano

International Journal of Molecular Sciences, Vol 21, Iss 3760, p

A Focus on Heme Metabolism and Fe-S Cluster Biogenesis

2020 Volume 3760

Abstract	Heme and Fe-S clusters regulate a plethora of essential biological processes ranging from cellular respiration and cell metabolism to the maintenance of genome integrity. Mutations in genes involved in heme metabolism and Fe-S cluster biogenesis cause different forms of ataxia, like posterior column ataxia and retinitis pigmentosa (PCARP), Friedreich’s ataxia (FRDA) and X-linked sideroblastic anemia with ataxia (XLSA/A). Despite great efforts in the elucidation of the molecular pathogenesis of these disorders several important questions still remain to be addressed. Starting with an overview of the biology of heme metabolism and Fe-S cluster biogenesis, the review discusses recent progress in the understanding of the molecular pathogenesis of PCARP, FRDA and XLSA/A, and highlights future line of research in the field. A better comprehension of the mechanisms leading to the degeneration of neural circuity responsible for balance and coordinated movement will be crucial for the therapeutic management of these patients.
Keywords	ataxia ; FLVCR1 ; FRATAXIN ; ABCB7 ; PCARP ; FRDA and XLSA/A ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2020-05-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Inhibition of Heme Export and/or Heme Synthesis Potentiates Metformin Anti-Proliferative Effect on Cancer Cell Lines.

Allocco, Anna Lucia / Bertino, Francesca / Petrillo, Sara / Chiabrando, Deborah / Riganti, Chiara / Bardelli, Alberto / Altruda, Fiorella / Fiorito, Veronica / Tolosano, Emanuela

Cancers

2022 Volume 14, Issue 5

Abstract: Cancer is one of the leading causes of mortality worldwide. Beyond standard therapeutic options, whose effectiveness is often reduced by drug resistance, repurposing of the antidiabetic drug metformin appears promising. Heme metabolism plays a pivotal ... ...

Abstract	Cancer is one of the leading causes of mortality worldwide. Beyond standard therapeutic options, whose effectiveness is often reduced by drug resistance, repurposing of the antidiabetic drug metformin appears promising. Heme metabolism plays a pivotal role in the control of metabolic adaptations that sustain cancer cell proliferation. Recently, we demonstrated the existence of a functional axis between the heme synthetic enzyme ALAS1 and the heme exporter FLVCR1a exploited by cancer cells to down-modulate oxidative metabolism. In colorectal cancer cell lines, the inhibition of heme synthesis-export system was associated with reduced proliferation and survival. Here, we aim to assess whether the inhibition of the heme synthesis-export system affects the sensitivity of colorectal cancer cells to metformin. Our data demonstrate that the inhibition of this system, either by blocking heme efflux with a
Language	English
Publishing date	2022-02-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers14051230
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Article: Mitochondrial Targeting in Neurodegeneration: A Heme Perspective.

Fiorito, Veronica / Chiabrando, Deborah / Tolosano, Emanuela

Pharmaceuticals (Basel, Switzerland)

2018 Volume 11, Issue 3

Abstract: Mitochondrial dysfunction has achieved an increasing interest in the field of neurodegeneration as a pathological hallmark for different disorders. The impact of mitochondria is related to a variety of mechanisms and several of them can co-exist in the ... ...

Abstract	Mitochondrial dysfunction has achieved an increasing interest in the field of neurodegeneration as a pathological hallmark for different disorders. The impact of mitochondria is related to a variety of mechanisms and several of them can co-exist in the same disease. The central role of mitochondria in neurodegenerative disorders has stimulated studies intended to implement therapeutic protocols based on the targeting of the distinct mitochondrial processes. The review summarizes the most relevant mechanisms by which mitochondria contribute to neurodegeneration, encompassing therapeutic approaches. Moreover, a new perspective is proposed based on the heme impact on neurodegeneration. The heme metabolism plays a central role in mitochondrial functions, and several evidences indicate that alterations of the heme metabolism are associated with neurodegenerative disorders. By reporting the body of knowledge on this topic, the review intends to stimulate future studies on the role of heme metabolism in neurodegeneration, envisioning innovative strategies in the struggle against neurodegenerative diseases.
Language	English
Publishing date	2018-09-18
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph11030087
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Article: Unraveling the Role of Heme in Neurodegeneration.

Chiabrando, Deborah / Fiorito, Veronica / Petrillo, Sara / Tolosano, Emanuela

Frontiers in neuroscience

2018 Volume 12, Page(s) 712

Abstract: Heme (iron-protoporphyrin IX) is an essential co-factor involved in several biological processes, including neuronal survival and differentiation. Nevertheless, an excess of free-heme promotes oxidative stress and lipid peroxidation, thus leading to cell ...

Abstract	Heme (iron-protoporphyrin IX) is an essential co-factor involved in several biological processes, including neuronal survival and differentiation. Nevertheless, an excess of free-heme promotes oxidative stress and lipid peroxidation, thus leading to cell death. The toxic properties of heme in the brain have been extensively studied during intracerebral or subarachnoid hemorrhages. Recently, a growing number of neurodegenerative disorders have been associated to alterations of heme metabolism. Hence, the etiology of such diseases remains undefined. The aim of this review is to highlight the neuropathological role of heme and to discuss the major heme-regulated pathways that might be crucial for the survival of neuronal cells. The understanding of the molecular mechanisms linking heme to neurodegeneration will be important for therapeutic purposes.
Language	English
Publishing date	2018-10-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2018.00712
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Article ; Online: Expression and purification of the heme exporter FLVCR1a.

Chiabrando, Deborah / Scietti, Luigi / Prajica, Adriana Georgiana / Bertino, Francesca / Tolosano, Emanuela / Magnani, Francesca

Protein expression and purification

2020 Volume 172, Page(s) 105637

Abstract: With many crucial roles in enzymatic aerobic metabolism, the concentration of the heme must be tightly regulated. The heme exporter Feline Leukemia Virus sub-group C Receptor 1a (FLVCR1a), an integral membrane protein with twelve transmembrane helices, ... ...

Abstract	With many crucial roles in enzymatic aerobic metabolism, the concentration of the heme must be tightly regulated. The heme exporter Feline Leukemia Virus sub-group C Receptor 1a (FLVCR1a), an integral membrane protein with twelve transmembrane helices, is a key player in the maintenance of cellular heme homeostasis. It was first identified as the host receptor for the Feline Leukemia Virus sub-group C (FeLV-C), a retrovirus causing hematological abnormalities in cats and other felines. Mutations in the Flvcr1 were later identified in human patients affected by Posterior Column Ataxia and Retinitis Pigmentosa (PCARP) and Hereditary Sensory and Autonomic Neuropathies (HSANs). Despite being an essential component in heme balance, currently there is a lack in the understanding of its function at the molecular level, including the effect of disease-causing mutations on protein function and structure. Therefore, there is a need for protocols to achieve efficient recombinant production yielding milligram amounts of highly pure protein to be used for biochemical and structural studies. Here, we report the first FLVCR1a reliable protocol suitable for both antibody generation and structural characterisation.
MeSH term(s)	Animals ; Carrier Proteins/biosynthesis ; Carrier Proteins/chemistry ; Carrier Proteins/genetics ; Carrier Proteins/isolation & purification ; Cats ; Gene Expression ; Heme ; Humans ; Membrane Transport Proteins/biosynthesis ; Membrane Transport Proteins/chemistry ; Membrane Transport Proteins/genetics ; Membrane Transport Proteins/isolation & purification ; Mice ; Receptors, Virus/biosynthesis ; Receptors, Virus/chemistry ; Receptors, Virus/genetics ; Receptors, Virus/isolation & purification ; Recombinant Proteins/biosynthesis ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/isolation & purification
Chemical Substances	Carrier Proteins ; Flvcr1 protein, mouse ; Membrane Transport Proteins ; Receptors, Virus ; Recombinant Proteins ; Heme (42VZT0U6YR)
Language	English
Publishing date	2020-04-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1055455-5
ISSN	1096-0279 ; 1046-5928
ISSN (online)	1096-0279
ISSN	1046-5928
DOI	10.1016/j.pep.2020.105637
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Article ; Online: Mitochondrial Targeting in Neurodegeneration

Veronica Fiorito / Deborah Chiabrando / Emanuela Tolosano

Pharmaceuticals, Vol 11, Iss 3, p

A Heme Perspective

2018 Volume 87

Abstract	Mitochondrial dysfunction has achieved an increasing interest in the field of neurodegeneration as a pathological hallmark for different disorders. The impact of mitochondria is related to a variety of mechanisms and several of them can co-exist in the same disease. The central role of mitochondria in neurodegenerative disorders has stimulated studies intended to implement therapeutic protocols based on the targeting of the distinct mitochondrial processes. The review summarizes the most relevant mechanisms by which mitochondria contribute to neurodegeneration, encompassing therapeutic approaches. Moreover, a new perspective is proposed based on the heme impact on neurodegeneration. The heme metabolism plays a central role in mitochondrial functions, and several evidences indicate that alterations of the heme metabolism are associated with neurodegenerative disorders. By reporting the body of knowledge on this topic, the review intends to stimulate future studies on the role of heme metabolism in neurodegeneration, envisioning innovative strategies in the struggle against neurodegenerative diseases.
Keywords	neurodegeneration ; mitochondria ; therapy ; heme ; haem ; Medicine ; R ; Pharmacy and materia medica ; RS1-441
Subject code	610
Language	English
Publishing date	2018-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Duality of Nrf2 in iron-overload cardiomyopathy.

Federti, Enrica / Vinchi, Francesca / Iatcenko, Iana / Ghigo, Alessandra / Matte, Alessandro / Toya, Serge Cedrick Mbiandjeu / Siciliano, Angela / Chiabrando, Deborah / Tolosano, Emanuela / Vance, Steven Zebulon / Riccardi, Veronica / Andolfo, Immacolata / Iezzi, Manuela / Lamolinara, Alessia / Iolascon, Achille / De Franceschi, Lucia

Haematologica

2023 Volume 108, Issue 5, Page(s) 1335–1348

Abstract: Cardiomyopathy deeply affects quality of life and mortality of patients with b-thalassemia or with transfusion-dependent myelodysplastic syndromes. Recently, a link between Nrf2 activity and iron metabolism has been reported in liver ironoverload murine ... ...

Abstract	Cardiomyopathy deeply affects quality of life and mortality of patients with b-thalassemia or with transfusion-dependent myelodysplastic syndromes. Recently, a link between Nrf2 activity and iron metabolism has been reported in liver ironoverload murine models. Here, we studied C57B6 mice as healthy control and nuclear erythroid factor-2 knockout (Nrf2-/-) male mice aged 4 and 12 months. Eleven-month-old wild-type and Nrf2-/- mice were fed with either standard diet or a diet containing 2.5% carbonyl-iron (iron overload [IO]) for 4 weeks. We show that Nrf2-/- mice develop an age-dependent cardiomyopathy, characterized by severe oxidation, degradation of SERCA2A and iron accumulation. This was associated with local hepcidin expression and increased serum non-transferrin-bound iron, which promotes maladaptive cardiac remodeling and interstitial fibrosis related to overactivation of the TGF-b pathway. When mice were exposed to IO diet, the absence of Nrf2 was paradoxically protective against further heart iron accumulation. Indeed, the combination of prolonged oxidation and the burst induced by IO diet resulted in activation of the unfolded protein response (UPR) system, which in turn promotes hepcidin expression independently from heart iron accumulation. In the heart of Hbbth3/+ mice, a model of b-thalassemia intermedia, despite the activation of Nrf2 pathway, we found severe protein oxidation, activation of UPR system and cardiac fibrosis independently from heart iron content. We describe the dual role of Nrf2 when aging is combined with IO and its novel interrelation with UPR system to ensure cell survival. We open a new perspective for early and intense treatment of cardiomyopathy in patients with b-thalassemia before the appearance of heart iron accumulation.
MeSH term(s)	Animals ; Male ; Mice ; Cardiomyopathies/etiology ; Cardiomyopathies/genetics ; Cardiomyopathies/metabolism ; Hepcidins ; Iron/metabolism ; Iron Overload/complications ; Iron Overload/genetics ; Iron Overload/metabolism ; NF-E2-Related Factor 2/metabolism ; Quality of Life ; Thalassemia/complications ; Thalassemia/genetics ; Thalassemia/metabolism
Chemical Substances	Hepcidins ; Iron (E1UOL152H7) ; NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse
Language	English
Publishing date	2023-05-01
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2022.281995
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