2020
DOI: 10.3390/ijms21176134
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Correction: Sunzini, F., et al. Hydrogen Sulfide as a Potential Regulatory Gasotransmitter in Arthritic Diseases. Int. J. Mol. Sci. 2020, 21, 1180; doi:10.3390/ijms21041180

Abstract: The authors wish to make the following correction to this paper [...]

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Cited by 4 publications
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“…[ 8 ] Many experiments confirmed H 2 S simulated tissue and biological functions in the human body, such as inhibiting the inflammatory response, [ 9 ] and importantly, expanding plasma IL‐10 levels, while suppressing the accumulation of lipopolysaccharide (LPS)‐induced neutrophils plasma interleukin‐1 (IL‐1β), [ 10 ] and tumor necrosis factor‐α (TNF‐α). [ 11 ] Hydrogen sulfide is not applied in the clinic directly because of the high toxicity associated with the uncontrollable release of this gas. In this regard, H 2 S donors have emerged as potential convenient substitutes for direct H 2 S dosing.…”
Section: Introductionmentioning
confidence: 99%
“…[ 8 ] Many experiments confirmed H 2 S simulated tissue and biological functions in the human body, such as inhibiting the inflammatory response, [ 9 ] and importantly, expanding plasma IL‐10 levels, while suppressing the accumulation of lipopolysaccharide (LPS)‐induced neutrophils plasma interleukin‐1 (IL‐1β), [ 10 ] and tumor necrosis factor‐α (TNF‐α). [ 11 ] Hydrogen sulfide is not applied in the clinic directly because of the high toxicity associated with the uncontrollable release of this gas. In this regard, H 2 S donors have emerged as potential convenient substitutes for direct H 2 S dosing.…”
Section: Introductionmentioning
confidence: 99%
“…21 However, dysregulation of endogenous H 2 S emerges in various diseases such as diabetes, cancer and enteritis, and specifically, leads to inflammatory exacerbation by upregulating inflammatory cytokine expression in RA. 22,23 Under RA conditions, the over-expressed endogenous H 2 S acts as a pro-inflammatory mediator to stimulate mitogen-activated protein kinases (MAPK), which upregulate several adhesion molecules such as intercellular adhesion molecule (ICAM-1) [24][25][26][27] and eventually induce macrophage inflammatory cytokine expression. [28][29][30] In this way, modulation of the endogenous H 2 S level becomes a potential target for halting inflammatory progression by suppression of the cytokine level.…”
Section: Introductionmentioning
confidence: 99%