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Article ; Online: The potential of the novel NAD

Chiang, Shannon / Kalinowski, Danuta S / Dharmasivam, Mahendiran / Braidy, Nady / Richardson, Des R / Huang, Michael L H

Pharmacological research

2020 Volume 155, Page(s) 104680

Abstract: Friedreich's ataxia (FA) is due to deficiency of the mitochondrial protein, frataxin, which results in multiple pathologies including a deadly, hypertrophic cardiomyopathy. Frataxin loss leads to deleterious accumulations of redox-active, mitochondrial ... ...

Abstract	Friedreich's ataxia (FA) is due to deficiency of the mitochondrial protein, frataxin, which results in multiple pathologies including a deadly, hypertrophic cardiomyopathy. Frataxin loss leads to deleterious accumulations of redox-active, mitochondrial iron, and suppressed mitochondrial bioenergetics. Hence, there is an urgent need to develop innovative pharmaceuticals. Herein, the activity of the novel compound, 6-methoxy-2-salicylaldehyde nicotinoyl hydrazone (SNH6), was assessed in vivo using the well-characterized muscle creatine kinase (MCK) conditional frataxin knockout (KO) mouse model of FA. The design of SNH6 incorporated a dual-mechanism mediating: (1) NAD
MeSH term(s)	Adenosine Triphosphate/metabolism ; Aldehydes/pharmacology ; Aldehydes/therapeutic use ; Animals ; Cardiomyopathies/drug therapy ; Cardiomyopathies/metabolism ; Cell Line ; Creatine Kinase, MM Form/genetics ; Disease Models, Animal ; Friedreich Ataxia/drug therapy ; Friedreich Ataxia/metabolism ; Hydrazones/pharmacology ; Hydrazones/therapeutic use ; Iron/metabolism ; Iron Chelating Agents/pharmacology ; Iron Chelating Agents/therapeutic use ; Iron-Binding Proteins/genetics ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria, Heart/drug effects ; Mitochondria, Heart/metabolism ; NAD/metabolism ; Rats ; Frataxin
Chemical Substances	6-methoxy-2-salicylaldehyde nicotinoyl hydrazone ; Aldehydes ; Hydrazones ; Iron Chelating Agents ; Iron-Binding Proteins ; NAD (0U46U6E8UK) ; Adenosine Triphosphate (8L70Q75FXE) ; Iron (E1UOL152H7) ; Creatine Kinase, MM Form (EC 2.7.3.2)
Language	English
Publishing date	2020-02-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2020.104680
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Article ; Online: The growing evidence for targeting P-glycoprotein in lysosomes to overcome resistance.

Stefan, Sven Marcel / Jansson, Patric J / Kalinowski, Danuta S / Anjum, Rukhsana / Dharmasivam, Mahendiran / Richardson, Des R

Future medicinal chemistry

2020 Volume 12, Issue 6, Page(s) 473–477

MeSH term(s)	ATP Binding Cassette Transporter, Subfamily B, Member 1/antagonists & inhibitors ; ATP Binding Cassette Transporter, Subfamily B, Member 1/metabolism ; Animals ; Antineoplastic Agents/pharmacology ; Drug Resistance, Multiple/drug effects ; Drug Resistance, Neoplasm/drug effects ; Humans ; Lysosomes/chemistry ; Lysosomes/metabolism ; Thiosemicarbazones/pharmacology
Chemical Substances	ATP Binding Cassette Transporter, Subfamily B, Member 1 ; Antineoplastic Agents ; Thiosemicarbazones
Language	English
Publishing date	2020-02-26
Publishing country	England
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Review
ISSN	1756-8927
ISSN (online)	1756-8927
DOI	10.4155/fmc-2019-0350
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Article: Tumor-induced neoangiogenesis and receptor tyrosine kinases – Mechanisms and strategies for acquired resistance

Yunus, Madiha / Jansson, Patric J / Kovacevic, Zaklina / Kalinowski, Danuta S / Richardson, Des R

Biochimica et biophysica acta. 2019 July, v. 1863, no. 7

2019

Abstract: Angiogenesis is essential for tumor growth, proliferation and metastasis. Tumor-related angiogenesis is complex and involves multiple signaling pathways. Controlling angiogenesis is a promising strategy for limiting cancer progression.Several receptor ... ...

Abstract	Angiogenesis is essential for tumor growth, proliferation and metastasis. Tumor-related angiogenesis is complex and involves multiple signaling pathways. Controlling angiogenesis is a promising strategy for limiting cancer progression.Several receptor tyrosine kinases influence the angiogenic response via multiple signaling molecules and pathways. Understanding the functional interaction of kinases in the angiogenic process and development of resistance to kinase inhibition is essential for future successful therapeutic strategies.Strategies that target receptor tyrosine kinases and other tumor microenvironment factors simultaneously, or sequentially, are required for achieving an efficient and robust anti-angiogenic response.Understanding the molecular mechanism of angiogenesis has improved, and has led, to the clinical development and approval of anti-angiogenic drugs. While many patients have benefited from these agents, their limited efficacy and the development of resistance remains a challenge. This review highlights current therapies and challenges associated with targeting angiogenesis in cancer.
Keywords	angiogenesis ; drugs ; enzyme inhibition ; metastasis ; neoplasms ; patients ; receptor protein-tyrosine kinase ; signal transduction ; therapeutics
Language	English
Dates of publication	2019-07
Size	p. 1217-1225.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	840755-1
ISSN	0304-4165
ISSN	0304-4165
DOI	10.1016/j.bbagen.2019.04.017
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Tumor-induced neoangiogenesis and receptor tyrosine kinases - Mechanisms and strategies for acquired resistance.

Yunus, Madiha / Jansson, Patric J / Kovacevic, Zaklina / Kalinowski, Danuta S / Richardson, Des R

Biochimica et biophysica acta. General subjects

2019 Volume 1863, Issue 7, Page(s) 1217–1225

Abstract: Background: Angiogenesis is essential for tumor growth, proliferation and metastasis. Tumor-related angiogenesis is complex and involves multiple signaling pathways. Controlling angiogenesis is a promising strategy for limiting cancer progression.: ... ...

Abstract	Background: Angiogenesis is essential for tumor growth, proliferation and metastasis. Tumor-related angiogenesis is complex and involves multiple signaling pathways. Controlling angiogenesis is a promising strategy for limiting cancer progression. Scope of review: Several receptor tyrosine kinases influence the angiogenic response via multiple signaling molecules and pathways. Understanding the functional interaction of kinases in the angiogenic process and development of resistance to kinase inhibition is essential for future successful therapeutic strategies. Major conclusions: Strategies that target receptor tyrosine kinases and other tumor microenvironment factors simultaneously, or sequentially, are required for achieving an efficient and robust anti-angiogenic response. General significance: Understanding the molecular mechanism of angiogenesis has improved, and has led, to the clinical development and approval of anti-angiogenic drugs. While many patients have benefited from these agents, their limited efficacy and the development of resistance remains a challenge. This review highlights current therapies and challenges associated with targeting angiogenesis in cancer.
MeSH term(s)	Drug Resistance, Neoplasm ; Humans ; Neoplasms/blood supply ; Neoplasms/enzymology ; Neovascularization, Pathologic ; Receptor Protein-Tyrosine Kinases/metabolism
Chemical Substances	Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
Language	English
Publishing date	2019-04-25
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	60-7
ISSN	1872-8006 ; 1879-2596 ; 1879-260X ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1872-8006 ; 1879-2596 ; 1879-260X ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbagen.2019.04.017
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Article: Unraveling the mysteries of serum albumin-more than just a serum protein.

Merlot, Angelica M / Kalinowski, Danuta S / Richardson, Des R

Frontiers in physiology

2014 Volume 5, Page(s) 299

Abstract: Serum albumin is a multi-functional protein that is able to bind and transport numerous endogenous and exogenous compounds. The development of albumin drug carriers is gaining increasing importance in the targeted delivery of cancer therapy, particularly ...

Abstract	Serum albumin is a multi-functional protein that is able to bind and transport numerous endogenous and exogenous compounds. The development of albumin drug carriers is gaining increasing importance in the targeted delivery of cancer therapy, particularly as a result of the market approval of the paclitaxel-loaded albumin nanoparticle, Abraxane®. Considering this, there is renewed interest in isolating and characterizing albumin-binding proteins or receptors on the plasma membrane that are responsible for albumin uptake. Initially, the cellular uptake and intracellular localization of albumin was unknown due to the large confinement of the protein within the vascular and interstitial compartment of the body. Studies have since assessed the intracellular localization of albumin in order to understand the mechanisms and pathways responsible for its uptake, distribution and catabolism in multiple tissues, and this is reviewed herein.
Language	English
Publishing date	2014-08-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2014.00299
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Article ; Online: Synthesis, Characterization, and in Vitro Anticancer Activity of Copper and Zinc Bis(Thiosemicarbazone) Complexes.

Anjum, Rukhsana / Palanimuthu, Duraippandi / Kalinowski, Danuta S / Lewis, William / Park, Kyung Chan / Kovacevic, Zaklina / Khan, Irfan Ullah / Richardson, Des R

Inorganic chemistry

2019 Volume 58, Issue 20, Page(s) 13709–13723

Abstract: A series of eight bis(thiosemicarbazone) ligands and 16 of their respective copper(II) and zinc(II) complexes containing a combination of hydrogen, methyl, pyridyl, phenyl, and/or ethyl substituents at the diimine position of the ligand backbone were ... ...

Abstract	A series of eight bis(thiosemicarbazone) ligands and 16 of their respective copper(II) and zinc(II) complexes containing a combination of hydrogen, methyl, pyridyl, phenyl, and/or ethyl substituents at the diimine position of the ligand backbone were synthesized and characterized. The objective of this study was to identify the structure-activity relationships within a series of analogues with different substituents at the diimine position of the backbone and at the terminal N atom. The Cu(II) complexes Cu(GTSM
MeSH term(s)	Antineoplastic Agents/chemical synthesis ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Cell Proliferation/drug effects ; Coordination Complexes/chemical synthesis ; Coordination Complexes/chemistry ; Coordination Complexes/pharmacology ; Copper/chemistry ; Copper/pharmacology ; Crystallography, X-Ray ; Dose-Response Relationship, Drug ; Drug Screening Assays, Antitumor ; Humans ; Models, Molecular ; Molecular Structure ; Structure-Activity Relationship ; Thiosemicarbazones/chemistry ; Thiosemicarbazones/pharmacology ; Tumor Cells, Cultured ; Zinc/chemistry ; Zinc/pharmacology
Chemical Substances	Antineoplastic Agents ; Coordination Complexes ; Thiosemicarbazones ; Copper (789U1901C5) ; Zinc (J41CSQ7QDS)
Language	English
Publishing date	2019-07-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	1484438-2
ISSN	1520-510X ; 0020-1669
ISSN (online)	1520-510X
ISSN	0020-1669
DOI	10.1021/acs.inorgchem.9b01281
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Article ; Online: Mitochondrial dysfunction in the neuro-degenerative and cardio-degenerative disease, Friedreich's ataxia.

Chiang, Shannon / Kalinowski, Danuta S / Jansson, Patric J / Richardson, Des R / Huang, Michael L-H

Neurochemistry international

2017 Volume 117, Page(s) 35–48

Abstract: Mitochondrial homeostasis is essential for maintaining healthy cellular function and survival. The detrimental involvement of mitochondrial dysfunction in neuro-degenerative diseases has recently been highlighted in human conditions, such as Parkinson's, ...

Abstract	Mitochondrial homeostasis is essential for maintaining healthy cellular function and survival. The detrimental involvement of mitochondrial dysfunction in neuro-degenerative diseases has recently been highlighted in human conditions, such as Parkinson's, Alzheimer's and Huntington's disease. Friedreich's ataxia (FA) is another neuro-degenerative, but also cardio-degenerative condition, where mitochondrial dysfunction plays a crucial role in disease progression. Deficient expression of the mitochondrial protein, frataxin, is the primary cause of FA, which leads to adverse alterations in whole cell and mitochondrial iron metabolism. Dys-regulation of iron metabolism in these compartments, results in the accumulation of inorganic iron deposits in the mitochondrial matrix that is thought to potentiate oxidative damage observed in FA. Therefore, the maintenance of mitochondrial homeostasis is crucial in the progression of neuro-degenerative conditions, particularly in FA. In this review, vital mitochondrial homeostatic processes and their roles in FA pathogenesis will be discussed. These include mitochondrial iron processing, mitochondrial dynamics (fusion and fission processes), mitophagy, mitochondrial biogenesis, mitochondrial energy production and calcium metabolism.
MeSH term(s)	Animals ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Friedreich Ataxia/genetics ; Friedreich Ataxia/metabolism ; Friedreich Ataxia/pathology ; Homeostasis/physiology ; Humans ; Iron-Binding Proteins/genetics ; Iron-Binding Proteins/metabolism ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondria/pathology ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Oxidative Stress/physiology ; Frataxin
Chemical Substances	Iron-Binding Proteins
Language	English
Publishing date	2017-08-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	283190-9
ISSN	1872-9754 ; 0197-0186
ISSN (online)	1872-9754
ISSN	0197-0186
DOI	10.1016/j.neuint.2017.08.002
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Article ; Online: Ascorbate and Tumor Cell Iron Metabolism: The Evolving Story and Its Link to Pathology.

Bae, Dong-Hun / Gholam Azad, Mahan / Kalinowski, Danuta S / Lane, Darius J R / Jansson, Patric J / Richardson, Des R

Antioxidants & redox signaling

2019 Volume 33, Issue 12, Page(s) 816–838

Abstract: Significance: ...

Abstract	Significance:
MeSH term(s)	Ascorbic Acid/metabolism ; Autophagy ; Biomarkers ; Disease Susceptibility ; Energy Metabolism ; Humans ; Hydrogen Peroxide/metabolism ; Iron/metabolism ; Neoplasms/drug therapy ; Neoplasms/etiology ; Neoplasms/metabolism ; Neoplasms/pathology ; Polyamines/metabolism
Chemical Substances	Biomarkers ; Polyamines ; Hydrogen Peroxide (BBX060AN9V) ; Iron (E1UOL152H7) ; Ascorbic Acid (PQ6CK8PD0R)
Language	English
Publishing date	2019-12-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2019.7903
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Article ; Online: The Role of the Antioxidant Response in Mitochondrial Dysfunction in Degenerative Diseases: Cross-Talk between Antioxidant Defense, Autophagy, and Apoptosis.

Huang, Michael L-H / Chiang, Shannon / Kalinowski, Danuta S / Bae, Dong-Hun / Sahni, Sumit / Richardson, Des R

Oxidative medicine and cellular longevity

2019 Volume 2019, Page(s) 6392763

Abstract: The mitochondrion is an essential organelle important for the generation of ATP for cellular function. This is especially critical for cells with high energy demands, such as neurons for signal transmission and cardiomyocytes for the continuous ... ...

Abstract	The mitochondrion is an essential organelle important for the generation of ATP for cellular function. This is especially critical for cells with high energy demands, such as neurons for signal transmission and cardiomyocytes for the continuous mechanical work of the heart. However, deleterious reactive oxygen species are generated as a result of mitochondrial electron transport, requiring a rigorous activation of antioxidative defense in order to maintain homeostatic mitochondrial function. Indeed, recent studies have demonstrated that the dysregulation of antioxidant response leads to mitochondrial dysfunction in human degenerative diseases affecting the nervous system and the heart. In this review, we outline and discuss the mitochondrial and oxidative stress factors causing degenerative diseases, such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and Friedreich's ataxia. In particular, the pathological involvement of mitochondrial dysfunction in relation to oxidative stress, energy metabolism, mitochondrial dynamics, and cell death will be explored. Understanding the pathology and the development of these diseases has highlighted novel regulators in the homeostatic maintenance of mitochondria. Importantly, this offers potential therapeutic targets in the development of future treatments for these degenerative diseases.
MeSH term(s)	Antioxidants/metabolism ; Apoptosis ; Autophagy ; Energy Metabolism ; Heredodegenerative Disorders, Nervous System/metabolism ; Heredodegenerative Disorders, Nervous System/pathology ; Humans ; Mitochondria/metabolism ; Mitochondria/pathology ; Neurons/metabolism ; Neurons/pathology ; Oxidative Stress ; Reactive Oxygen Species/metabolism
Chemical Substances	Antioxidants ; Reactive Oxygen Species
Language	English
Publishing date	2019-04-07
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1942-0994
ISSN (online)	1942-0994
DOI	10.1155/2019/6392763
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Article ; Online: Novel chelators for cancer treatment: where are we now?

Merlot, Angelica M / Kalinowski, Danuta S / Richardson, Des R

Antioxidants & redox signaling

2013 Volume 18, Issue 8, Page(s) 973–1006

Abstract: Significance: Under normal circumstances, cellular iron levels are tightly regulated due to the potential toxic effects of this metal ion. There is evidence that tumors possess altered iron homeostasis, which is mediated by the perturbed expression of ... ...

Abstract	Significance: Under normal circumstances, cellular iron levels are tightly regulated due to the potential toxic effects of this metal ion. There is evidence that tumors possess altered iron homeostasis, which is mediated by the perturbed expression of iron-related proteins, for example, transferrin receptor 1, ferritin and ferroportin 1. The de-regulation of iron homeostasis in cancer cells reveals a particular vulnerability to iron-depletion using iron chelators. In this review, we examine the absorption of iron from the gut; its transport, metabolism, and homeostasis in mammals; and the molecular pathways involved. Additionally, evidence for alterations in iron processing in cancer are described along with the perturbations in other biologically important transition metal ions, for example, copper(II) and zinc(II). These changes can be therapeutically manipulated by the use of novel chelators that have recently been shown to be highly effective in terms of inhibiting tumor growth. Recent advances: Such chelators include those of the thiosemicarbazone class that were originally thought to target only ribonucleotide reductase, but are now known to have multiple effects, including the generation of cytotoxic radicals. Critical issues: Several chelators have shown marked anti-tumor activity in vivo against a variety of solid tumors. An important aspect is the toxicology and the efficacy of these agents in clinical trials. Future directions: As part of the process of the clinical assessment of the new chelators, an extensive toxicological assessment in multiple animal models is essential for designing appropriate dosing protocols in humans.
MeSH term(s)	Animals ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Chelating Agents/chemistry ; Chelating Agents/pharmacology ; Chelating Agents/therapeutic use ; Coordination Complexes/metabolism ; Humans ; Iron/metabolism ; Iron Chelating Agents/chemistry ; Iron Chelating Agents/pharmacology ; Iron Chelating Agents/therapeutic use ; Metals/metabolism ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Oxidation-Reduction/drug effects
Chemical Substances	Antineoplastic Agents ; Chelating Agents ; Coordination Complexes ; Iron Chelating Agents ; Metals ; Iron (E1UOL152H7)
Language	English
Publishing date	2013-03-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1483836-9
ISSN	1557-7716 ; 1523-0864
ISSN (online)	1557-7716
ISSN	1523-0864
DOI	10.1089/ars.2012.4540
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