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Article ; Online: A comparison of the chemical biology of hydropersulfides (RSSH) with other protective biological antioxidants and nucleophiles.

Fukuto, Jon M / Hobbs, Adrian J

2020 Volume 107, Page(s) 46–57

Abstract: The hydropersulfide (RSSH) functional group has received significant recent interest due to its unique chemical properties that set it apart from other biological species. The chemistry of RSSH predicts that one possible biological role may be as a ... ...

Abstract	The hydropersulfide (RSSH) functional group has received significant recent interest due to its unique chemical properties that set it apart from other biological species. The chemistry of RSSH predicts that one possible biological role may be as a protectant against cellular oxidative and electrophilic stress. That is, RSSH has reducing and nucleophilic properties that may combat the potentially destructive biochemistry of toxicologically relevant oxidants and electrophiles. However, there are currently numerous other molecules that have established roles in this regard. For example, ascorbate and tocopherols are potent antioxidants that quench deleterious oxidative reactions and glutathione (GSH) is a well-established and highly prevalent biological protectant against electrophile toxicity. Thus, in order to begin to understand the possible role of RSSH species as protectants against oxidative/electrophilic stress, the inherent chemical properties of RSSH versus these other protectants will be discussed and contrasted.
MeSH term(s)	Animals ; Antioxidants/chemistry ; Antioxidants/physiology ; Ascorbic Acid/chemistry ; Ascorbic Acid/physiology ; Glutathione/chemistry ; Glutathione/physiology ; Humans ; Hydrogen Sulfide/chemistry ; Hydrogen Sulfide/metabolism ; Nitric Oxide/chemistry ; Nitric Oxide/physiology ; Oxidation-Reduction ; Oxidative Stress/physiology ; Sulfides/chemistry ; Sulfides/metabolism
Chemical Substances	Antioxidants ; Sulfides ; persulfides ; Nitric Oxide (31C4KY9ESH) ; Glutathione (GAN16C9B8O) ; Ascorbic Acid (PQ6CK8PD0R) ; Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2020-11-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1362794-6
ISSN	1089-8611 ; 1089-8603
ISSN (online)	1089-8611
ISSN	1089-8603
DOI	10.1016/j.niox.2020.11.004
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Article ; Online: Guanylyl cyclase can't stand the HETE.

Hobbs, Adrian J

American journal of physiology. Heart and circulatory physiology

2016 Volume 310, Issue 11, Page(s) H1608–10

MeSH term(s)	Guanylate Cyclase ; Hydroxyeicosatetraenoic Acids
Chemical Substances	Hydroxyeicosatetraenoic Acids ; Guanylate Cyclase (EC 4.6.1.2)
Language	English
Publishing date	2016-05-03
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	603838-4
ISSN	1522-1539 ; 0363-6135
ISSN (online)	1522-1539
ISSN	0363-6135
DOI	10.1152/ajpheart.00326.2016
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Article ; Online: A Janus-Faced Role for Atrial Natriuretic Peptide in Myocardial Infarction?

Hobbs, Adrian J

Circulation research

2016 Volume 119, Issue 2, Page(s) 181–183

MeSH term(s)	Atrial Natriuretic Factor ; Cyclic GMP ; Guanylate Cyclase ; Humans ; Myocardial Infarction ; Natriuretic Peptide, C-Type ; Receptors, Atrial Natriuretic Factor
Chemical Substances	Natriuretic Peptide, C-Type (127869-51-6) ; Atrial Natriuretic Factor (85637-73-6) ; Guanylate Cyclase (EC 4.6.1.2) ; Receptors, Atrial Natriuretic Factor (EC 4.6.1.2) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2016-07-09
Publishing country	United States
Document type	Editorial ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.116.309119
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Article ; Online: C-type Natriuretic Peptide: A Multifaceted Paracrine Regulator in the Heart and Vasculature.

Moyes, Amie J / Hobbs, Adrian J

International journal of molecular sciences

2019 Volume 20, Issue 9

Abstract: C-type natriuretic peptide (CNP) is an autocrine and paracrine mediator released by endothelial cells, cardiomyocytes and fibroblasts that regulates vital physiological functions in the cardiovascular system. These roles are conveyed via two cognate ... ...

Abstract	C-type natriuretic peptide (CNP) is an autocrine and paracrine mediator released by endothelial cells, cardiomyocytes and fibroblasts that regulates vital physiological functions in the cardiovascular system. These roles are conveyed via two cognate receptors, natriuretic peptide receptor B (NPR-B) and natriuretic peptide receptor C (NPR-C), which activate different signalling pathways that mediate complementary yet distinct cellular responses. Traditionally, CNP has been deemed the endothelial component of the natriuretic peptide system, while its sibling peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), are considered the endocrine guardians of cardiac function and blood volume. However, accumulating evidence indicates that CNP not only modulates vascular tone and blood pressure, but also governs a wide range of cardiovascular effects including the control of inflammation, angiogenesis, smooth muscle and endothelial cell proliferation, atherosclerosis, cardiomyocyte contractility, hypertrophy, fibrosis, and cardiac electrophysiology. This review will focus on the novel physiological functions ascribed to CNP, the receptors/signalling mechanisms involved in mediating its cardioprotective effects, and the development of therapeutics targeting CNP signalling pathways in different disease pathologies.
MeSH term(s)	Atrial Natriuretic Factor/genetics ; Cardiovascular System/metabolism ; Cardiovascular System/pathology ; Endothelial Cells/metabolism ; Ethanolamines/metabolism ; Humans ; Myocardium/metabolism ; Myocytes, Cardiac/metabolism ; Natriuretic Peptide, Brain/genetics ; Natriuretic Peptide, C-Type/genetics ; Natriuretic Peptide, C-Type/metabolism ; Paracrine Communication/genetics ; Phenethylamines/metabolism ; Receptors, Atrial Natriuretic Factor/genetics
Chemical Substances	Ethanolamines ; Phenethylamines ; Natriuretic Peptide, Brain (114471-18-0) ; Natriuretic Peptide, C-Type (127869-51-6) ; Atrial Natriuretic Factor (85637-73-6) ; Receptors, Atrial Natriuretic Factor (EC 4.6.1.2) ; atrial natriuretic factor receptor B (EC 4.6.1.2) ; atrial natriuretic factor receptor C (EC 4.6.1.2) ; bamethan (Y08ZFJ9TFK)
Language	English
Publishing date	2019-05-08
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/ijms20092281
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Article ; Online: Multiplicity of Nitric Oxide and Natriuretic Peptide Signaling in Heart Failure.

Preedy, Michael E J / Baliga, Reshma S / Hobbs, Adrian J

Journal of cardiovascular pharmacology

2019 Volume 75, Issue 5, Page(s) 370–384

Abstract: Heart failure (HF) is a common consequence of several cardiovascular diseases and is understood as a vicious cycle of cardiac and hemodynamic decline. The current inventory of treatments either alleviates the pathophysiological features (eg, cardiac ... ...

Abstract	Heart failure (HF) is a common consequence of several cardiovascular diseases and is understood as a vicious cycle of cardiac and hemodynamic decline. The current inventory of treatments either alleviates the pathophysiological features (eg, cardiac dysfunction, neurohumoral activation, and ventricular remodeling) and/or targets any underlying pathologies (eg, hypertension and myocardial infarction). Yet, since these do not provide a cure, the morbidity and mortality associated with HF remains high. Therefore, the disease constitutes an unmet medical need, and novel therapies are desperately needed. Cyclic guanosine-3',5'-monophosphate (cGMP), synthesized by nitric oxide (NO)- and natriuretic peptide (NP)-responsive guanylyl cyclase (GC) enzymes, exerts numerous protective effects on cardiac contractility, hypertrophy, fibrosis, and apoptosis. Impaired cGMP signaling, which can occur after GC deactivation and the upregulation of cyclic nucleotide-hydrolyzing phosphodiesterases (PDEs), promotes cardiac dysfunction. In this study, we review the role that NO/cGMP and NP/cGMP signaling plays in HF. After considering disease etiology, the physiological effects of cGMP in the heart are discussed. We then assess the evidence from preclinical models and patients that compromised cGMP signaling contributes to the HF phenotype. Finally, the potential of pharmacologically harnessing cardioprotective cGMP to rectify the present paucity of effective HF treatments is examined.
MeSH term(s)	Animals ; Cardiovascular Agents/therapeutic use ; Cyclic GMP/metabolism ; Guanylate Cyclase/metabolism ; Heart Failure/drug therapy ; Heart Failure/metabolism ; Heart Failure/physiopathology ; Humans ; Molecular Targeted Therapy ; Myocardial Contraction ; Myocardium/metabolism ; Natriuretic Peptides/metabolism ; Nitric Oxide/metabolism ; Phosphoric Diester Hydrolases/metabolism ; Second Messenger Systems/drug effects ; Ventricular Function, Left ; Ventricular Remodeling
Chemical Substances	Cardiovascular Agents ; Natriuretic Peptides ; Nitric Oxide (31C4KY9ESH) ; Phosphoric Diester Hydrolases (EC 3.1.4.-) ; Guanylate Cyclase (EC 4.6.1.2) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2019-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391970-5
ISSN	1533-4023 ; 0160-2446
ISSN (online)	1533-4023
ISSN	0160-2446
DOI	10.1097/FJC.0000000000000724
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Article: Hydropersulfides (RSSH) and Nitric Oxide (NO) Signaling: Possible Effects on S-Nitrosothiols (RS-NO)

Fukuto, Jon M. / Perez-Ternero, Cristina / Zarenkiewicz, Jessica / Lin, Joseph / Hobbs, Adrian J. / Toscano, John P.

Antioxidants. 2022 Jan. 16, v. 11, no. 1

2022

Abstract: S-Nitrosothiol (RS-NO) formation in proteins and peptides have been implicated as factors in the etiology of many diseases and as possible regulators of thiol protein function. They have also been proposed as possible storage forms of nitric oxide (NO). ... ...

Abstract	S-Nitrosothiol (RS-NO) formation in proteins and peptides have been implicated as factors in the etiology of many diseases and as possible regulators of thiol protein function. They have also been proposed as possible storage forms of nitric oxide (NO). However, despite their proposed functions/roles, there appears to be little consensus regarding the physiological mechanisms of RS-NO formation and degradation. Hydropersulfides (RSSH) have recently been discovered as endogenously generated species with unique reactivity. One important reaction of RSSH is with RS-NO, which leads to the degradation of RS-NO as well as the release of NO. Thus, it can be speculated that RSSH can be a factor in the regulation of steady-state RS-NO levels, and therefore may be important in RS-NO (patho)physiology. Moreover, RSSH-mediated NO release from RS-NO may be a possible mechanism allowing RS-NO to serve as a storage form of NO.
Keywords	etiology ; nitric oxide ; peptides ; physiology ; thiols
Language	English
Dates of publication	2022-0116
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11010169
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Animal models of pulmonary hypertension: Getting to the heart of the problem.

Dignam, Joshua P / Scott, Tara E / Kemp-Harper, Barbara K / Hobbs, Adrian J

British journal of pharmacology

2021 Volume 179, Issue 5, Page(s) 811–837

Abstract: Despite recent therapeutic advances, pulmonary hypertension (PH) remains a fatal disease due to the development of right ventricular (RV) failure. At present, no treatments targeted at the right ventricle are available, and RV function is not widely ... ...

Abstract	Despite recent therapeutic advances, pulmonary hypertension (PH) remains a fatal disease due to the development of right ventricular (RV) failure. At present, no treatments targeted at the right ventricle are available, and RV function is not widely considered in the preclinical assessment of new therapeutics. Several small animal models are used in the study of PH, including the classic models of exposure to either hypoxia or monocrotaline, newer combinational and genetic models, and pulmonary artery banding, a surgical model of pure RV pressure overload. These models reproduce selected features of the structural remodelling and functional decline seen in patients and have provided valuable insight into the pathophysiology of RV failure. However, significant reversal of remodelling and improvement in RV function remains a therapeutic obstacle. Emerging animal models will provide a deeper understanding of the mechanisms governing the transition from adaptive remodelling to a failing right ventricle, aiding the hunt for druggable molecular targets. LINKED ARTICLES: This article is part of a themed issue on Preclinical Models for Cardiovascular disease research (BJP 75th Anniversary). To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.5/issuetoc.
MeSH term(s)	Animals ; Disease Models, Animal ; Heart Failure ; Humans ; Hypertension, Pulmonary/drug therapy ; Monocrotaline ; Pulmonary Artery ; Ventricular Dysfunction, Right/drug therapy ; Ventricular Function, Right
Chemical Substances	Monocrotaline (73077K8HYV)
Language	English
Publishing date	2021-05-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.15444
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Article ; Online: The role of cGMP signalling in auditory processing in health and disease.

Marchetta, Philine / Rüttiger, Lukas / Hobbs, Adrian J / Singer, Wibke / Knipper, Marlies

British journal of pharmacology

2021 Volume 179, Issue 11, Page(s) 2378–2393

Abstract: cGMP is generated by the cGMP-forming guanylyl cyclases (GCs), the intracellular nitric oxide (NO)-sensitive (soluble) guanylyl cyclase (sGC) and transmembrane GC (e.g. GC-A and GC-B). In summarizing the particular role of cGMP signalling for hearing, we ...

Abstract	cGMP is generated by the cGMP-forming guanylyl cyclases (GCs), the intracellular nitric oxide (NO)-sensitive (soluble) guanylyl cyclase (sGC) and transmembrane GC (e.g. GC-A and GC-B). In summarizing the particular role of cGMP signalling for hearing, we show that GC generally do not interfere significantly with basic hearing function but rather sustain a healthy state for proper temporal coding, fast discrimination and adjustments during injury. sGC is critical for the integrity of the first synapse in the ascending auditory pathway, the inner hair cell synapse. GC-A promotes hair cell stability under stressful conditions such as acoustic trauma or ageing. GC-B plays a role in the development of efferent feed-back and gain control. Regarding the crucial role hearing has for language development, speech discrimination and cognitive brain functions, differential pharmaceutical targeting of GCs offers therapeutic promise for the restoration of hearing. LINKED ARTICLES: This article is part of a themed issue on cGMP Signalling in Cell Growth and Survival. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.11/issuetoc.
MeSH term(s)	Auditory Perception ; Cyclic GMP/metabolism ; Guanylate Cyclase/metabolism ; Nitric Oxide/metabolism ; Signal Transduction ; Soluble Guanylyl Cyclase/metabolism
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; Guanylate Cyclase (EC 4.6.1.2) ; Soluble Guanylyl Cyclase (EC 4.6.1.2) ; Cyclic GMP (H2D2X058MU)
Language	English
Publishing date	2021-05-04
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.15455
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Article ; Online: Innovative Anti-Inflammatory and Pro-resolving Strategies for Pulmonary Hypertension: High Blood Pressure Research Council of Australia Award 2019.

Scott, Tara E / Qin, Cheng Xue / Drummond, Grant R / Hobbs, Adrian J / Kemp-Harper, Barbara K

Hypertension (Dallas, Tex. : 1979)

2021 Volume 78, Issue 5, Page(s) 1168–1184

Abstract: Pulmonary hypertension is a rare, ostensibly incurable, and etiologically diverse disease with an unacceptably high 5-year mortality rate (≈50%), worse than many cancers. Irrespective of pathogenic origin, dysregulated immune processes underlie pulmonary ...

Abstract	Pulmonary hypertension is a rare, ostensibly incurable, and etiologically diverse disease with an unacceptably high 5-year mortality rate (≈50%), worse than many cancers. Irrespective of pathogenic origin, dysregulated immune processes underlie pulmonary hypertension pathobiology, particularly pertaining to pulmonary vascular remodeling. As such, a variety of proinflammatory pathways have been mooted as novel therapeutic targets. One such pathway involves the family of innate immune regulators known as inflammasomes. In addition, a new and emerging concept is differentiating between anti-inflammatory approaches versus those that promote pro-resolving pathways. This review will briefly introduce inflammasomes and examine recent literature concerning their role in pulmonary hypertension. Moreover, it will explore the difference between inflammation-suppressing and pro-resolution approaches and how this links to inflammasomes. Finally, we will investigate new avenues for targeting inflammation in pulmonary hypertension via more targeted anti-inflammatory or inflammation resolving strategies.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/therapeutic use ; Australia ; Awards and Prizes ; Blood Pressure/drug effects ; Blood Pressure/physiology ; Humans ; Hypertension, Pulmonary/drug therapy ; Hypertension, Pulmonary/metabolism ; Hypertension, Pulmonary/physiopathology ; Inflammasomes/drug effects ; Inflammasomes/metabolism ; Inflammation/metabolism ; Inflammation/physiopathology ; Inflammation/prevention & control ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
Chemical Substances	Anti-Inflammatory Agents ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein
Language	English
Publishing date	2021-09-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	423736-5
ISSN	1524-4563 ; 0194-911X ; 0362-4323
ISSN (online)	1524-4563
ISSN	0194-911X ; 0362-4323
DOI	10.1161/HYPERTENSIONAHA.120.14525
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Article: Hydropersulfides (RSSH) and Nitric Oxide (NO) Signaling: Possible Effects on S-Nitrosothiols (RS-NO).

Fukuto, Jon M / Perez-Ternero, Cristina / Zarenkiewicz, Jessica / Lin, Joseph / Hobbs, Adrian J / Toscano, John P

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 1

Abstract	S-Nitrosothiol (RS-NO) formation in proteins and peptides have been implicated as factors in the etiology of many diseases and as possible regulators of thiol protein function. They have also been proposed as possible storage forms of nitric oxide (NO). However, despite their proposed functions/roles, there appears to be little consensus regarding the physiological mechanisms of RS-NO formation and degradation. Hydropersulfides (RSSH) have recently been discovered as endogenously generated species with unique reactivity. One important reaction of RSSH is with RS-NO, which leads to the degradation of RS-NO as well as the release of NO. Thus, it can be speculated that RSSH can be a factor in the regulation of steady-state RS-NO levels, and therefore may be important in RS-NO (patho)physiology. Moreover, RSSH-mediated NO release from RS-NO may be a possible mechanism allowing RS-NO to serve as a storage form of NO.
Language	English
Publishing date	2022-01-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11010169
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