Hydrogen Sulfide and its Interaction with Other Players in Inflammation

Manandhar, Sumeet; Sinha, Poonam; Ejiwale, Grace; Bhatia, Madhav

doi:10.1007/978-981-16-0991-6_6

Cited by 8 publications

(6 citation statements)

References 244 publications

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“…As indicated by its definition, sepsis is characterized by aberrant systematic inflammation and associated organ injury in response to a local infection. Increasing investigations have been pointing to the multifaceted actions played by the SP–NK1R system in sepsis-related inflammatory organ injuries, including lung injury, liver injury, and kidney injury [ 69 , 71 ].…”

Section: Substance P and Its Receptors In Inflammation-associated Org...mentioning

confidence: 99%

Inflammation and Organ Injury the Role of Substance P and Its Receptors

Zhu

Bhatia

2023

IJMS

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Tightly controlled inflammation is an indispensable mechanism in the maintenance of cellular and organismal homeostasis in living organisms. However, aberrant inflammation is detrimental and has been suggested as a key contributor to organ injury with different etiologies. Substance P (SP) is a neuropeptide with a robust effect on inflammation. The proinflammatory effects of SP are achieved by activating its functional receptors, namely the neurokinin 1 receptor (NK1R) receptor and mas-related G protein-coupled receptors X member 2 (MRGPRX2) and its murine homolog MRGPRB2. Upon activation, the receptors further signal to several cellular signaling pathways involved in the onset, development, and progression of inflammation. Therefore, excessive SP–NK1R or SP–MRGPRX2/B2 signals have been implicated in the pathogenesis of inflammation-associated organ injury. In this review, we summarize our current knowledge of SP and its receptors and the emerging roles of the SP–NK1R system and the SP–MRGPRX2/B2 system in inflammation and injury in multiple organs resulting from different pathologies. We also briefly discuss the prospect of developing a therapeutic strategy for inflammatory organ injury by disrupting the proinflammatory actions of SP via pharmacological intervention.

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Section: Substance P and Its Receptors In Inflammation-associated Org...mentioning

confidence: 99%

Inflammation and Organ Injury the Role of Substance P and Its Receptors

Zhu

Bhatia

2023

IJMS

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“…Notably, similar to NO, H 2 S is discovered to be an important endogenous epigenetic modulator [ 51 ]. Aberrant H 2 S metabolism occurs in many pathological states, such as sepsis, inflammation, coronavirus disease 2019, hypertension, atherosclerosis, obstructive respiratory disease, lung injury, macrophage activation, retinal diseases and neurodegenerative disease [ 77 , 81 , 86 , 87 , 88 , 89 ].…”

Section: Gaseous Mediatorsmentioning

confidence: 99%

“…Accumulating evidence has pointed to the crosstalk among NO, CO and H 2 S [ 86 , 90 ]. To date, four interaction mechanisms have been identified, which are competition/synergy for heme in heme-containing proteins, modulation of the generation of other gases and competition for post-translational modification sites in proteins and formation of hybrid molecules [ 91 , 92 , 93 ].…”

Section: Gaseous Mediatorsmentioning

confidence: 99%

Gases in Sepsis: Novel Mediators and Therapeutic Targets

Zhu

Chambers

Zeng

et al. 2022

IJMS

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Sepsis, a potentially lethal condition resulting from failure to control the initial infection, is associated with a dysregulated host defense response to pathogens and their toxins. Sepsis remains a leading cause of morbidity, mortality and disability worldwide. The pathophysiology of sepsis is very complicated and is not yet fully understood. Worse still, the development of effective therapeutic agents is still an unmet need and a great challenge. Gases, including nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H2S), are small-molecule biological mediators that are endogenously produced, mainly by enzyme-catalyzed reactions. Accumulating evidence suggests that these gaseous mediators are widely involved in the pathophysiology of sepsis. Many sepsis-associated alterations, such as the elimination of invasive pathogens, the resolution of disorganized inflammation and the preservation of the function of multiple organs and systems, are shaped by them. Increasing attention has been paid to developing therapeutic approaches targeting these molecules for sepsis/septic shock, taking advantage of the multiple actions played by NO, CO and H2S. Several preliminary studies have identified promising therapeutic strategies for gaseous-mediator-based treatments for sepsis. In this review article, we summarize the state-of-the-art knowledge on the pathophysiology of sepsis; the metabolism and physiological function of NO, CO and H2S; the crosstalk among these gaseous mediators; and their crucial effects on the development and progression of sepsis. In addition, we also briefly discuss the prospect of developing therapeutic interventions targeting these gaseous mediators for sepsis.

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“…Taking advantage of the development of chemical and genetic H 2 S research tools and the recognition of the nature of being a molecular signaling mediator of H 2 S, the complex roles of H 2 S in a plethora of acute/chronic inflammatory conditions, such as pulmonary diseases (see the detailed discussion in Section 4 ), gastrointestinal disorders, sepsis (systematic inflammation) and arthritis (local inflammation), have been substantially investigated and become increasingly clear [ 27 , 28 , 60 ]. However, the precise role of H 2 S in the inflammatory process is still ambiguous and yet to be fully understood as both pro-inflammatory and anti-inflammatory properties of H 2 S have been proposed [ 28 , 60 , 61 ].…”

Section: Cross-linking Of H 2 S With Cell Death Ox...mentioning

confidence: 99%

Hydrogen Sulfide: A Gaseous Mediator and Its Key Role in Programmed Cell Death, Oxidative Stress, Inflammation and Pulmonary Disease

2022

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Hydrogen sulfide (H2S) has been acknowledged as a novel gaseous mediator. The metabolism of H2S in mammals is tightly controlled and is mainly achieved by many physiological reactions catalyzed by a suite of enzymes. Although the precise actions of H2S in regulating programmed cell death, oxidative stress and inflammation are yet to be fully understood, it is becoming increasingly clear that H2S is extensively involved in these crucial processes. Since programmed cell death, oxidative stress and inflammation have been demonstrated as three important mechanisms participating in the pathogenesis of various pulmonary diseases, it can be inferred that aberrant H2S metabolism also functions as a critical contributor to pulmonary diseases, which has also been extensively investigated. In the meantime, substantial attention has been paid to developing therapeutic approaches targeting H2S for pulmonary diseases. In this review, we summarize the cutting-edge knowledge on the metabolism of H2S and the relevance of H2S to programmed cell death, oxidative stress and inflammation. We also provide an update on the crucial roles played by H2S in the pathogenesis of several pulmonary diseases. Finally, we discuss the perspective on targeting H2S metabolism in the treatment of pulmonary diseases.

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Hydrogen Sulfide and its Interaction with Other Players in Inflammation

Cited by 8 publications

References 244 publications

Inflammation and Organ Injury the Role of Substance P and Its Receptors

Inflammation and Organ Injury the Role of Substance P and Its Receptors

Gases in Sepsis: Novel Mediators and Therapeutic Targets

Hydrogen Sulfide: A Gaseous Mediator and Its Key Role in Programmed Cell Death, Oxidative Stress, Inflammation and Pulmonary Disease

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