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Biomolecules
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Biomolecules Controlling Transition Metals Derangement and Metal-Based Compounds as Therapeutic...
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Biomolecules Controlling Transition Metals Derangement and Metal-Based Compounds as Therapeutic Approach for Cancer and Neurodegeneration

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 18194

Special Issue Editors

Dr. Luisa Rossi

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Guest Editor
Department of Biology, Tor Vergata University of Rome, Rome, Italy
Interests: copper; oxidative stress; mitochondria; neurodegeneration; proteins; biochemistry; enzymes
Special Issues, Collections and Topics in MDPI journals
Dr. Rosanna Squitti

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Guest Editor
AFaR Fatebenefratelli Hosp San Giovanni Calibita, Dept Neurosci, Rome, Italy
Interests: copper; metal; ceruloplasmin; cognition; synaptic plasticity
Special Issues, Collections and Topics in MDPI journals
Dr. Anastasia De Luca

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Guest Editor
Department of Biology, Tor Vergata University of Rome, Rome, Italy
Interests: cancer; copper signaling; EMT; metastasis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alteration of the essential metals iron (Fe) and copper (Cu) homeostasis could play a pivotal role in the most relevant challenge for human health, cancer and neurodegeneration, although the precise mechanisms involved are not clear. For instance, in Alzheimer’s disease, copper and iron contribute to the formation of the amyloid plaques, and ferroptosis is related to pathological cell death. Moreover, copper-binding proteins (i.e., MEMO1, LOX family members, MEK1, XIAP) and iron-regulated genes (i.e., TfR1, FTL chain, IRP2, Lcn-2) are involved in cancer progression. On the other hand, several studies demonstrate that metal-based compounds and synthetic or metal-binding molecules of nutritional origin exert anti-cancer and neuroprotective action. For example, plant polyphenols are known to bind metals, and the resulting complexes silence the redox-related toxicity of metals or promote their pro-oxidant activity. This Special Issue aims to collect the most recent work in this field, in order to prompt further research, to pinpoint novel metal-based mechanisms underlying neurodegeneration and cancer, and to detail the chemistry of transition metal chelators and their mechanism of action.

Dr. Luisa Rossi
Dr. Rosanna Squitti
Dr. Anastasia De Luca
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • transition metals
  • iron
  • copper
  • neurodegeneration
  • cancer
  • metal complexes
  • nutraceuticals

Published Papers (4 papers)

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Review

23 pages, 1445 KiB  
Review
Role of Oxidative Stress in the Pathogenesis of Amyotrophic Lateral Sclerosis: Antioxidant Metalloenzymes and Therapeutic Strategies
by Pavlína Hemerková and Martin Vališ
Biomolecules 2021, 11(3), 437; https://doi.org/10.3390/biom11030437 - 16 Mar 2021
Cited by 28 | Viewed by 3565
Abstract
Amyotrophic lateral sclerosis (ALS) affects motor neurons in the cerebral cortex, brainstem and spinal cord and leads to death due to respiratory failure within three to five years. Although the clinical symptoms of this disease were first described in 1869 and it is [...] Read more.
Amyotrophic lateral sclerosis (ALS) affects motor neurons in the cerebral cortex, brainstem and spinal cord and leads to death due to respiratory failure within three to five years. Although the clinical symptoms of this disease were first described in 1869 and it is the most common motor neuron disease and the most common neurodegenerative disease in middle-aged individuals, the exact etiopathogenesis of ALS remains unclear and it remains incurable. However, free oxygen radicals (i.e., molecules containing one or more free electrons) are known to contribute to the pathogenesis of this disease as they very readily bind intracellular structures, leading to functional impairment. Antioxidant enzymes, which are often metalloenzymes, inactivate free oxygen radicals by converting them into a less harmful substance. One of the most important antioxidant enzymes is Cu2+Zn2+ superoxide dismutase (SOD1), which is mutated in 20% of cases of the familial form of ALS (fALS) and up to 7% of sporadic ALS (sALS) cases. In addition, the proper functioning of catalase and glutathione peroxidase (GPx) is essential for antioxidant protection. In this review article, we focus on the mechanisms through which these enzymes are involved in the antioxidant response to oxidative stress and thus the pathogenesis of ALS and their potential as therapeutic targets. Full article
(This article belongs to the Special Issue Biomolecules Controlling Transition Metals Derangement and Metal-Based Compounds as Therapeutic Approach for Cancer and Neurodegeneration)
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14 pages, 1289 KiB  
Review
Ferroptosis in Friedreich’s Ataxia: A Metal-Induced Neurodegenerative Disease
by Piergiorgio La Rosa, Sara Petrillo, Maria Teresa Fiorenza, Enrico Silvio Bertini and Fiorella Piemonte
Biomolecules 2020, 10(11), 1551; https://doi.org/10.3390/biom10111551 - 13 Nov 2020
Cited by 22 | Viewed by 4117
Abstract
Ferroptosis is an iron-dependent form of regulated cell death, arising from the accumulation of lipid-based reactive oxygen species when glutathione-dependent repair systems are compromised. Lipid peroxidation, mitochondrial impairment and iron dyshomeostasis are the hallmark of ferroptosis, which is emerging as a crucial player [...] Read more.
Ferroptosis is an iron-dependent form of regulated cell death, arising from the accumulation of lipid-based reactive oxygen species when glutathione-dependent repair systems are compromised. Lipid peroxidation, mitochondrial impairment and iron dyshomeostasis are the hallmark of ferroptosis, which is emerging as a crucial player in neurodegeneration. This review provides an analysis of the most recent advances in ferroptosis, with a special focus on Friedreich’s Ataxia (FA), the most common autosomal recessive neurodegenerative disease, caused by reduced levels of frataxin, a mitochondrial protein involved in iron–sulfur cluster synthesis and antioxidant defenses. The hypothesis is that the iron-induced oxidative damage accumulates over time in FA, lowering the ferroptosis threshold and leading to neuronal cell death and, at last, to cardiac failure. The use of anti-ferroptosis drugs combined with treatments able to activate the antioxidant response will be of paramount importance in FA therapy, such as in many other neurodegenerative diseases triggered by oxidative stress. Full article
(This article belongs to the Special Issue Biomolecules Controlling Transition Metals Derangement and Metal-Based Compounds as Therapeutic Approach for Cancer and Neurodegeneration)
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15 pages, 612 KiB  
Review
An Overview of the Ferroptosis Hallmarks in Friedreich’s Ataxia
by Riccardo Turchi, Raffaella Faraonio, Daniele Lettieri-Barbato and Katia Aquilano
Biomolecules 2020, 10(11), 1489; https://doi.org/10.3390/biom10111489 - 28 Oct 2020
Cited by 22 | Viewed by 4494
Abstract
Background: Friedreich’s ataxia (FRDA) is a neurodegenerative disease characterized by early mortality due to hypertrophic cardiomyopathy. FRDA is caused by reduced levels of frataxin (FXN), a mitochondrial protein involved in the synthesis of iron-sulphur clusters, leading to iron accumulation at the mitochondrial level, [...] Read more.
Background: Friedreich’s ataxia (FRDA) is a neurodegenerative disease characterized by early mortality due to hypertrophic cardiomyopathy. FRDA is caused by reduced levels of frataxin (FXN), a mitochondrial protein involved in the synthesis of iron-sulphur clusters, leading to iron accumulation at the mitochondrial level, uncontrolled production of reactive oxygen species and lipid peroxidation. These features are also common to ferroptosis, an iron-mediated type of cell death triggered by accumulation of lipoperoxides with distinct morphological and molecular characteristics with respect to other known cell deaths. Scope of review: Even though ferroptosis has been associated with various neurodegenerative diseases including FRDA, the mechanisms leading to disease onset/progression have not been demonstrated yet. We describe the molecular alterations occurring in FRDA that overlap with those characterizing ferroptosis. Major conclusions: The study of ferroptotic pathways is necessary for the understanding of FRDA pathogenesis, and anti-ferroptotic drugs could be envisaged as therapeutic strategies to cure FRDA. Full article
(This article belongs to the Special Issue Biomolecules Controlling Transition Metals Derangement and Metal-Based Compounds as Therapeutic Approach for Cancer and Neurodegeneration)
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17 pages, 498 KiB  
Review
Zinc Therapy in Early Alzheimer’s Disease: Safety and Potential Therapeutic Efficacy
by Rosanna Squitti, Amit Pal, Mario Picozza, Abofazl Avan, Mariacarla Ventriglia, Mauro C. Rongioletti and Tjaard Hoogenraad
Biomolecules 2020, 10(8), 1164; https://doi.org/10.3390/biom10081164 - 09 Aug 2020
Cited by 23 | Viewed by 5335
Abstract
Zinc therapy is normally utilized for treatment of Wilson disease (WD), an inherited condition that is characterized by increased levels of non-ceruloplasmin bound (‘free’) copper in serum and urine. A subset of patients with Alzheimer’s disease (AD) or its prodromal form, known as [...] Read more.
Zinc therapy is normally utilized for treatment of Wilson disease (WD), an inherited condition that is characterized by increased levels of non-ceruloplasmin bound (‘free’) copper in serum and urine. A subset of patients with Alzheimer’s disease (AD) or its prodromal form, known as Mild Cognitive Impairment (MCI), fail to maintain a normal copper metabolic balance and exhibit higher than normal values of non-ceruloplasmin copper. Zinc’s action mechanism involves the induction of intestinal cell metallothionein, which blocks copper absorption from the intestinal tract, thus restoring physiological levels of non-ceruloplasmin copper in the body. On this basis, it is employed in WD. Zinc therapy has shown potential beneficial effects in preliminary AD clinical trials, even though the studies have missed their primary endpoints, since they have study design and other important weaknesses. Nevertheless, in the studied AD patients, zinc effectively decreased non-ceruloplasmin copper levels and showed potential for improved cognitive performances with no major side effects. This review discusses zinc therapy safety and the potential therapeutic effects that might be expected on a subset of individuals showing both cognitive complaints and signs of copper imbalance. Full article
(This article belongs to the Special Issue Biomolecules Controlling Transition Metals Derangement and Metal-Based Compounds as Therapeutic Approach for Cancer and Neurodegeneration)
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