About this Research Topic
In animals sulfur is an essential element, it is absorbed from the digestive tract in the form of sulfur amino acids, methionine and cysteine, of which methionine is an essential amino acid, while cysteine can be produced endogenously from methionine. The reactivity of the thiol group causes these compounds serve a variety of different functions in the cell including metal-binding possibility, maintain redox homeostasis, participation in signaling processes and protection against oxidative stress. The most abundant non-protein thiols include a tripeptide glutathione (GSH) and cysteine (Cys). GSH is an important intracellular low molecular antioxidant and its role in maintaining favorable redox status in cells is crucial. Cys can be used for protein synthesis but it is also a substrate for synthesis other important
sulfur-containing compounds with biological potentials – reactive sulfur species (RSS) including hydrogen sulfide (H2S) and compounds containing so-called sulfane sulfur:
persulfides and polysulfides.
Exploring the complex role of thiols and RSS in maintaining physiological processes as well as in pathology, like inflammation will provide novel pathophysiological insights and guide the development of more effective therapeutic strategies for treating inflammation and inflammatory disease. H2S has been recognized as the third gas signaling molecule,
following nitric oxide (NO) and carbon monoxide (CO). Recent evidence shows that H2S and other RSS are implicated in inflammatory responses. RSS and their donors/precursors exert antioxidative properties alleviating oxidative stress and inflammation; however, the mechanism of this phenomenon is still not completely explained. One of the mechanism of
RSS regulatory action is the persulfidation process, in which protein Cys thiols are converted to persulfides, affecting protein activity. It has been reorted that classical activation of
macrophages leads to widespread protein persulfidation. Therefore, sulfur-containing compounds in addition to their direct antioxidant activity can modulate endogenous
antioxidant systems.
This Research Topic aims to publish high-quality original research that highlights the interplay between sulfur-containing compounds and inflammatory processes. ”Sulfur
compounds and inflammation” is an increasingly hot topic, both in the diagnosis and prognosis of inflammatory diseases, but also in their development or treatment. We welcome
submissions focusing on, but not limited to:
• Physiological roles of endogenous thiols and RSS in inflammation and inflammatory
diseases
• Anti-inflammatory potential of various sulfur-containing compounds (i.e. lipoic acid, N-Acetylcysteine, disulfiram etc.)
• Therapeutic roles of H2S/RSS donors (synthetic and natural)
• The role of protein persulfidation in inflammation
• Eventual pro-inflammatory action of sulfur compounds
• The role of interaction between RSS and reactive oxygen or nitrogen species (ROS/RNS)
Please note that manuscripts describing the pharmacological action of drugs used in traditional medicine in models of disease, such as inflammatory disease, are not in scope unless they have a very strong focus on the immune system.
The Research Topic editors have no conflicts of interest to declare.
sulfur-containing compounds with biological potentials – reactive sulfur species (RSS) including hydrogen sulfide (H2S) and compounds containing so-called sulfane sulfur:
persulfides and polysulfides.
Exploring the complex role of thiols and RSS in maintaining physiological processes as well as in pathology, like inflammation will provide novel pathophysiological insights and guide the development of more effective therapeutic strategies for treating inflammation and inflammatory disease. H2S has been recognized as the third gas signaling molecule,
following nitric oxide (NO) and carbon monoxide (CO). Recent evidence shows that H2S and other RSS are implicated in inflammatory responses. RSS and their donors/precursors exert antioxidative properties alleviating oxidative stress and inflammation; however, the mechanism of this phenomenon is still not completely explained. One of the mechanism of
RSS regulatory action is the persulfidation process, in which protein Cys thiols are converted to persulfides, affecting protein activity. It has been reorted that classical activation of
macrophages leads to widespread protein persulfidation. Therefore, sulfur-containing compounds in addition to their direct antioxidant activity can modulate endogenous
antioxidant systems.
This Research Topic aims to publish high-quality original research that highlights the interplay between sulfur-containing compounds and inflammatory processes. ”Sulfur
compounds and inflammation” is an increasingly hot topic, both in the diagnosis and prognosis of inflammatory diseases, but also in their development or treatment. We welcome
submissions focusing on, but not limited to:
• Physiological roles of endogenous thiols and RSS in inflammation and inflammatory
diseases
• Anti-inflammatory potential of various sulfur-containing compounds (i.e. lipoic acid, N-Acetylcysteine, disulfiram etc.)
• Therapeutic roles of H2S/RSS donors (synthetic and natural)
• The role of protein persulfidation in inflammation
• Eventual pro-inflammatory action of sulfur compounds
• The role of interaction between RSS and reactive oxygen or nitrogen species (ROS/RNS)
Please note that manuscripts describing the pharmacological action of drugs used in traditional medicine in models of disease, such as inflammatory disease, are not in scope unless they have a very strong focus on the immune system.
The Research Topic editors have no conflicts of interest to declare.
Keywords: Hydrogen sulfide (H2S), inflammation, persulfides, polysulfides, protein persulfidation, reactive sulfur species, thiols
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
