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Article ; Online: Of Mice and Men: NAD

Chini, Eduardo Nunes

2020 Volume 31, Issue 6, Page(s) 1041–1043

Abstract: In this issue of Cell Metabolism, Pirinen et al. (2020) show that disruption in ... ...

Abstract	In this issue of Cell Metabolism, Pirinen et al. (2020) show that disruption in NAD
MeSH term(s)	Adult ; Homeostasis ; Humans ; Mitochondrial Myopathies/drug therapy ; Muscles ; NAD ; Niacin
Chemical Substances	NAD (0U46U6E8UK) ; Niacin (2679MF687A)
Language	English
Publishing date	2020-04-05
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2020.05.013
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Article ; Online: NAD metabolism: Role in senescence regulation and aging.

Chini, Claudia Christiano Silva / Cordeiro, Heidi Soares / Tran, Ngan Le Kim / Chini, Eduardo Nunes

Aging cell

2023 Volume 23, Issue 1, Page(s) e13920

Abstract: The geroscience hypothesis proposes that addressing the biology of aging could directly prevent the onset or mitigate the severity of multiple chronic diseases. Understanding the interplay between key aspects of the biological hallmarks of aging is ... ...

Abstract	The geroscience hypothesis proposes that addressing the biology of aging could directly prevent the onset or mitigate the severity of multiple chronic diseases. Understanding the interplay between key aspects of the biological hallmarks of aging is essential in delivering the promises of the geroscience hypothesis. Notably, the nucleotide nicotinamide adenine dinucleotide (NAD) interfaces with several biological hallmarks of aging, including cellular senescence, and changes in NAD metabolism have been shown to be involved in the aging process. The relationship between NAD metabolism and cellular senescence appears to be complex. On the one hand, the accumulation of DNA damage and mitochondrial dysfunction induced by low NAD
MeSH term(s)	NAD/metabolism ; Nucleotides ; Cellular Senescence
Chemical Substances	NAD (0U46U6E8UK) ; Nucleotides
Language	English
Publishing date	2023-07-09
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13920
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Zs.A 6581: Show issues

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Article ; Online: Implications of the PAPP-A-IGFBP-IGF-1 pathway in the pathogenesis and treatment of polycystic kidney disease.

Kashyap, Sonu / Zeidler, Julianna D / Chini, Claudia C S / Chini, Eduardo Nunes

Cellular signalling

2020 Volume 73, Page(s) 109698

Abstract: Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic diseases implicated in the development of end stage renal disease (ESRD). Although FDA has recently approved a drug against ADPKD, there is still a great need for ... ...

Abstract	Autosomal dominant polycystic kidney disease (ADPKD) is one of the most common genetic diseases implicated in the development of end stage renal disease (ESRD). Although FDA has recently approved a drug against ADPKD, there is still a great need for development of alternative management strategies for ADPKD. Understanding the different mechanisms that lead to cystogenesis and cyst expansion in ADPKD is imperative to develop new therapies against ADPKD. Recently, we demonstrated that caloric restriction can prevent the development of cystic disease in animal models of ADPKD and through these studies identified a new role for pregnancy associated plasma protein-A (PAPP-A), a component of the insulin-like growth factors (IGF) pathway, in the pathogenesis of this disease. The PAPP-A-IGF pathway plays an important role in regulation of cell growth, differentiation, and transformation and dysregulation of this pathway has been implicated in many diseases. Several indirect studies support the involvement of IGF-1 in the pathogenesis of ADPKD. However, it was only recently that we described a direct role for a component of this pathway in pathogenesis of ADPKD, opening a new avenue for the therapeutic approaches for this cystic disease. The present literature review will critically discuss the evidence that supports the role of components of IGF pathway in the pathogenesis of ADPKD and discuss the pharmacological implications of PAPP-A-IGF axis in this disease.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Proliferation ; Humans ; Insulin-Like Growth Factor Binding Proteins/metabolism ; Insulin-Like Growth Factor I/metabolism ; Polycystic Kidney, Autosomal Dominant/metabolism ; Polycystic Kidney, Autosomal Dominant/pathology ; Pregnancy-Associated Plasma Protein-A/physiology
Chemical Substances	IGF1 protein, human ; Insulin-Like Growth Factor Binding Proteins ; Insulin-Like Growth Factor I (67763-96-6) ; Pregnancy-Associated Plasma Protein-A (EC 3.4.24.-) ; PAPPA protein, human (EC 3.4.24.79)
Language	English
Publishing date	2020-06-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1002702-6
ISSN	1873-3913 ; 0898-6568
ISSN (online)	1873-3913
ISSN	0898-6568
DOI	10.1016/j.cellsig.2020.109698
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Article ; Online: Evolving concepts in NAD

Chini, Claudia C S / Zeidler, Julianna D / Kashyap, Sonu / Warner, Gina / Chini, Eduardo Nunes

Cell metabolism

2021 Volume 33, Issue 6, Page(s) 1076–1087

Abstract: NAD(H) and NADP(H) have traditionally been viewed as co-factors (or co-enzymes) involved in a myriad of oxidation-reduction reactions including the electron transport in the mitochondria. However, NAD pathway metabolites have many other important ... ...

Abstract	NAD(H) and NADP(H) have traditionally been viewed as co-factors (or co-enzymes) involved in a myriad of oxidation-reduction reactions including the electron transport in the mitochondria. However, NAD pathway metabolites have many other important functions, including roles in signaling pathways, post-translational modifications, epigenetic changes, and regulation of RNA stability and function via NAD-capping of RNA. Non-oxidative reactions ultimately lead to the net catabolism of these nucleotides, indicating that NAD metabolism is an extremely dynamic process. In fact, recent studies have clearly demonstrated that NAD has a half-life in the order of minutes in some tissues. Several evolving concepts on the metabolism, transport, and roles of these NAD pathway metabolites in disease states such as cancer, neurodegeneration, and aging have emerged in just the last few years. In this perspective, we discuss key recent discoveries and changing concepts in NAD metabolism and biology that are reshaping the field. In addition, we will pose some open questions in NAD biology, including why NAD metabolism is so fast and dynamic in some tissues, how NAD and its precursors are transported to cells and organelles, and how NAD metabolism is integrated with inflammation and senescence. Resolving these questions will lead to significant advancements in the field.
MeSH term(s)	Animals ; Energy Metabolism ; Humans ; Mitochondria/metabolism ; NAD/metabolism ; NADP/metabolism
Chemical Substances	NAD (0U46U6E8UK) ; NADP (53-59-8)
Language	English
Publishing date	2021-04-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2021.04.003
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Article ; Online: Implications of the NADase CD38 in COVID pathophysiology.

Zeidler, Julianna D / Kashyap, Sonu / Hogan, Kelly A / Chini, Eduardo Nunes

Physiological reviews

2021 Volume 102, Issue 1, Page(s) 339–341

Abstract: During the COVID-19 pandemic, efforts have been made worldwide to develop effective therapies to address the devastating immune-mediated effects of SARS-CoV-2. With the exception of monoclonal antibody-mediated therapeutics and preventive approaches such ...

Abstract	During the COVID-19 pandemic, efforts have been made worldwide to develop effective therapies to address the devastating immune-mediated effects of SARS-CoV-2. With the exception of monoclonal antibody-mediated therapeutics and preventive approaches such as mass immunization, most experimental or repurposed drugs have failed in large randomized clinical trials (https://www.who.int/publications/i/item/therapeutics-and-covid-19-living-guideline). The worldwide spread of SARS-CoV-2 virus revealed specific susceptibilities to the virus among the elderly and individuals with age-related syndromes. These populations were more likely to experience a hyperimmune response characterized by a treatment-resistant acute lung pathology accompanied by multiple organ failure. These observations underscore the interplay between the virus, the biology of aging, and outcomes observed in the most severe cases of SARS-CoV-2 infection. The ectoenzyme CD38 has been implicated in the process of "inflammaging" in aged tissues. In a current publication, Horenstein et al. present evidence to support the hypothesis that CD38 plays a central role in altered immunometabolism resulting from COVID-19 infection. The authors discuss a critical but underappreciated trifecta of CD38-mediated NAD
MeSH term(s)	ADP-ribosyl Cyclase 1/genetics ; ADP-ribosyl Cyclase 1/metabolism ; Aging ; COVID-19/physiopathology ; Gene Expression Regulation, Enzymologic ; Humans ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; NAD/metabolism ; SARS-CoV-2
Chemical Substances	Membrane Glycoproteins ; NAD (0U46U6E8UK) ; CD38 protein, human (EC 3.2.2.5) ; ADP-ribosyl Cyclase 1 (EC 3.2.2.6)
Language	English
Publishing date	2021-09-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	209902-0
ISSN	1522-1210 ; 0031-9333
ISSN (online)	1522-1210
ISSN	0031-9333
DOI	10.1152/physrev.00007.2021
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Article ; Online: Ecto-CD38-NADase inhibition modulates cardiac metabolism and protects mice against doxorubicin-induced cardiotoxicity.

Peclat, Thais R / Agorrody, Guillermo / Colman, Laura / Kashyap, Sonu / Zeidler, Julianna D / Chini, Claudia C S / Warner, Gina M / Thompson, Katie L / Dalvi, Pranjali / Beckedorff, Felipe / Ebtehaj, Sanam / Herrmann, Joerg / van Schooten, Wim / Chini, Eduardo Nunes

Cardiovascular research

2024 Volume 120, Issue 3, Page(s) 286–300

Abstract: Aims: Doxorubicin (DXR) is a chemotherapeutic agent that causes dose-dependent cardiotoxicity. Recently, it has been proposed that the NADase CD38 may play a role in doxorubicin-induced cardiotoxicity (DIC). CD38 is the main NAD+-catabolizing enzyme in ... ...

Abstract	Aims: Doxorubicin (DXR) is a chemotherapeutic agent that causes dose-dependent cardiotoxicity. Recently, it has been proposed that the NADase CD38 may play a role in doxorubicin-induced cardiotoxicity (DIC). CD38 is the main NAD+-catabolizing enzyme in mammalian tissues. Interestingly, in the heart, CD38 is mostly expressed as an ecto-enzyme that can be targeted by specific inhibitory antibodies. The goal of the present study is to characterize the role of CD38 ecto-enzymatic activity in cardiac metabolism and the development of DIC. Methods and results: Using both a transgenic animal model and a non-cytotoxic enzymatic anti-CD38 antibody, we investigated the role of CD38 and its ecto-NADase activity in DIC in pre-clinical models. First, we observed that DIC was prevented in the CD38 catalytically inactive (CD38-CI) transgenic mice. Both left ventricular systolic function and exercise capacity were decreased in wild-type but not in CD38-CI mice treated with DXR. Second, blocking CD38-NADase activity with the specific antibody 68 (Ab68) likewise protected mice against DIC and decreased DXR-related mortality by 50%. A reduction of DXR-induced mitochondrial dysfunction, energy deficiency, and inflammation gene expression were identified as the main mechanisms mediating the protective effects. Conclusion: NAD+-preserving strategies by inactivation of CD38 via a genetic or a pharmacological-based approach improve cardiac energetics and reduce cardiac inflammation and dysfunction otherwise seen in an acute DXR cardiotoxicity model.
MeSH term(s)	Mice ; Animals ; NAD+ Nucleosidase/metabolism ; ADP-ribosyl Cyclase 1/genetics ; ADP-ribosyl Cyclase 1/metabolism ; NAD/metabolism ; Cardiotoxicity ; Mice, Transgenic ; Doxorubicin/toxicity ; Inflammation ; Mammals/metabolism
Chemical Substances	NAD+ Nucleosidase (EC 3.2.2.5) ; ADP-ribosyl Cyclase 1 (EC 3.2.2.6) ; NAD (0U46U6E8UK) ; Doxorubicin (80168379AG)
Language	English
Publishing date	2024-01-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvae025
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Article ; Online: The NADase enzyme CD38: an emerging pharmacological target for systemic sclerosis, systemic lupus erythematosus and rheumatoid arthritis.

Peclat, Thais Ribeiro / Shi, Bo / Varga, John / Chini, Eduardo Nunes

Current opinion in rheumatology

2020 Volume 32, Issue 6, Page(s) 488–496

Abstract: Purpose of review: Here we review recent literature on the emerging role of nicotinamide adenine dinucleotide (NAD) metabolism and its dysfunction via the enzyme CD38 in the pathogenesis of rheumatologic diseases. We evaluate the potential of targeting ... ...

Abstract	Purpose of review: Here we review recent literature on the emerging role of nicotinamide adenine dinucleotide (NAD) metabolism and its dysfunction via the enzyme CD38 in the pathogenesis of rheumatologic diseases. We evaluate the potential of targeting CD38 to ameliorate NAD-related metabolic imbalance and tissue dysfunction in the treatment of systemic sclerosis (SSc), systemic lupus erythematous (SLE), and rheumatoid arthritis (RA). Recent findings: In this review, we will discuss emerging basic, preclinical, and human data that point to the novel role of CD38 in dysregulated NAD-homeostasis in SSc, SLE, and RA. In particular, recent studies implicate increased activity of CD38, one of the main enzymes in NAD catabolism, in the pathogenesis of persistent systemic fibrosis in SSc, and increased susceptibility of SLE patients to infections. We will also discuss recent studies that demonstrate that a cytotoxic CD38 antibody can promote clearance of plasma cells involved in the generation of RA antibodies. Summary: Recent studies identify potential therapeutic approaches for boosting NAD to treat rheumatologic diseases including SSc, RA, and SLE, with particular attention to inhibition of CD38 enzymatic activity as a target. Key future directions in the field include the determination of the cell-type specificity and role of CD38 enzymatic activity versus CD38 structural roles in human diseases, as well as the indicators and potential side effects of CD38-targeted treatments.
MeSH term(s)	ADP-ribosyl Cyclase 1/antagonists & inhibitors ; ADP-ribosyl Cyclase 1/metabolism ; Arthritis, Rheumatoid/immunology ; Arthritis, Rheumatoid/metabolism ; Humans ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/metabolism ; NAD+ Nucleosidase/metabolism ; Scleroderma, Systemic/immunology ; Scleroderma, Systemic/metabolism
Chemical Substances	NAD+ Nucleosidase (EC 3.2.2.5) ; ADP-ribosyl Cyclase 1 (EC 3.2.2.6)
Keywords	covid19
Language	English
Publishing date	2020-10-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1045317-9
ISSN	1531-6963 ; 1040-8711
ISSN (online)	1531-6963
ISSN	1040-8711
DOI	10.1097/BOR.0000000000000737
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Article ; Online: The CD38 glycohydrolase and the NAD sink: implications for pathological conditions.

Zeidler, Julianna D / Hogan, Kelly A / Agorrody, Guillermo / Peclat, Thais R / Kashyap, Sonu / Kanamori, Karina S / Gomez, Lilian Sales / Mazdeh, Delaram Z / Warner, Gina M / Thompson, Katie L / Chini, Claudia C S / Chini, Eduardo Nunes

American journal of physiology. Cell physiology

2022 Volume 322, Issue 3, Page(s) C521–C545

Abstract: Nicotinamide adenine dinucleotide (NAD) acts as a cofactor in several oxidation-reduction (redox) reactions and is a substrate for a number of nonredox enzymes. NAD is fundamental to a variety of cellular processes including energy metabolism, cell ... ...

Abstract	Nicotinamide adenine dinucleotide (NAD) acts as a cofactor in several oxidation-reduction (redox) reactions and is a substrate for a number of nonredox enzymes. NAD is fundamental to a variety of cellular processes including energy metabolism, cell signaling, and epigenetics. NAD homeostasis appears to be of paramount importance to health span and longevity, and its dysregulation is associated with multiple diseases. NAD metabolism is dynamic and maintained by synthesis and degradation. The enzyme CD38, one of the main NAD-consuming enzymes, is a key component of NAD homeostasis. The majority of CD38 is localized in the plasma membrane with its catalytic domain facing the extracellular environment, likely for the purpose of controlling systemic levels of NAD. Several cell types express CD38, but its expression predominates on endothelial cells and immune cells capable of infiltrating organs and tissues. Here we review potential roles of CD38 in health and disease and postulate ways in which CD38 dysregulation causes changes in NAD homeostasis and contributes to the pathophysiology of multiple conditions. Indeed, in animal models the development of infectious diseases, autoimmune disorders, fibrosis, metabolic diseases, and age-associated diseases including cancer, heart disease, and neurodegeneration are associated with altered CD38 enzymatic activity. Many of these conditions are modified in CD38-deficient mice or by blocking CD38 NADase activity. In diseases in which CD38 appears to play a role, CD38-dependent NAD decline is often a common denominator of pathophysiology. Thus, understanding dysregulation of NAD homeostasis by CD38 may open new avenues for the treatment of human diseases.
MeSH term(s)	ADP-ribosyl Cyclase 1/genetics ; ADP-ribosyl Cyclase 1/metabolism ; Animals ; Endothelial Cells/metabolism ; Glycoside Hydrolases ; Mice ; NAD/metabolism ; NAD+ Nucleosidase/metabolism
Chemical Substances	NAD (0U46U6E8UK) ; Glycoside Hydrolases (EC 3.2.1.-) ; NAD+ Nucleosidase (EC 3.2.2.5) ; ADP-ribosyl Cyclase 1 (EC 3.2.2.6)
Language	English
Publishing date	2022-02-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00451.2021
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Article ; Online: CD38 as a regulator of cellular NAD: a novel potential pharmacological target for metabolic conditions.

Chini, Eduardo Nunes

Current pharmaceutical design

2009 Volume 15, Issue 1, Page(s) 57–63

Abstract: CD38 is a multifunctional enzyme that uses nicotinamide adenine dinucleotide (NAD) as a substrate to generate second messengers. Recently, CD38 was also identified as one of the main cellular NADases in mammalian tissues and appears to regulate cellular ... ...

Abstract	CD38 is a multifunctional enzyme that uses nicotinamide adenine dinucleotide (NAD) as a substrate to generate second messengers. Recently, CD38 was also identified as one of the main cellular NADases in mammalian tissues and appears to regulate cellular levels of NAD in multiple tissues and cells. Due to the emerging role of NAD as a key molecule in multiple signaling pathways, and metabolic conditions it is imperative to determine the cellular mechanisms that regulate the synthesis and degradation of this nucleotide. In fact, recently it has been shown that NAD participates in multiple physiological processes such as insulin secretion, control of energy metabolism, neuronal and cardiac cell survival, airway constriction, asthma, aging and longevity. The discovery of CD38 as the main cellular NADase in mammalian tissues, and the characterization of its role on the control of cellular NAD levels indicate that CD38 may serve as a pharmacological target for multiple conditions.
MeSH term(s)	ADP-ribosyl Cyclase 1/metabolism ; Animals ; Humans ; Mice ; Molecular Structure ; NAD/chemistry ; NAD/metabolism ; Signal Transduction/physiology
Chemical Substances	NAD (0U46U6E8UK) ; ADP-ribosyl Cyclase 1 (EC 3.2.2.6)
Language	English
Publishing date	2009-01-16
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/138161209787185788
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Article: The NADase enzyme CD38: an emerging pharmacological target for systemic sclerosis, systemic lupus erythematosus and rheumatoid arthritis

Peclat, Thais Ribeiro / Shi, Bo / Varga, John / Chini, Eduardo Nunes

Curr Opin Rheumatol

Abstract: PURPOSE OF REVIEW: Here we review recent literature on the emerging role of nicotinamide adenine dinucleotide (NAD) metabolism and its dysfunction via the enzyme CD38 in the pathogenesis of rheumatologic diseases. We evaluate the potential of targeting ... ...

Abstract	PURPOSE OF REVIEW: Here we review recent literature on the emerging role of nicotinamide adenine dinucleotide (NAD) metabolism and its dysfunction via the enzyme CD38 in the pathogenesis of rheumatologic diseases. We evaluate the potential of targeting CD38 to ameliorate NAD-related metabolic imbalance and tissue dysfunction in the treatment of systemic sclerosis (SSc), systemic lupus erythematous (SLE), and rheumatoid arthritis (RA). RECENT FINDINGS: In this review, we will discuss emerging basic, preclinical, and human data that point to the novel role of CD38 in dysregulated NAD-homeostasis in SSc, SLE, and RA. In particular, recent studies implicate increased activity of CD38, one of the main enzymes in NAD catabolism, in the pathogenesis of persistent systemic fibrosis in SSc, and increased susceptibility of SLE patients to infections. We will also discuss recent studies that demonstrate that a cytotoxic CD38 antibody can promote clearance of plasma cells involved in the generation of RA antibodies. SUMMARY: Recent studies identify potential therapeutic approaches for boosting NAD to treat rheumatologic diseases including SSc, RA, and SLE, with particular attention to inhibition of CD38 enzymatic activity as a target. Key future directions in the field include the determination of the cell-type specificity and role of CD38 enzymatic activity versus CD38 structural roles in human diseases, as well as the indicators and potential side effects of CD38-targeted treatments.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #32941246
Database	COVID19

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