Hydrogen Sulfide and the Immune System

Rose, Peter; Zhu, Yi‐Zhun; Moore, Philip K.

doi:10.1007/978-981-16-0991-6_5

Cited by 8 publications

(3 citation statements)

References 241 publications

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“…cGAS inhibition reversed the myeloid lineage bias in MDS in mice. Furthermore, hydrogen sulfide (H 2 S, an anti-inflammatory molecule) also inhibits the cGAS/STING/NLRP3 axis to protect against choline-induced cardiotoxicity [206,207].…”

Section: Alr and Nlr Interaction With Cgas/sting Signalingmentioning

confidence: 99%

cGLRs Join Their Cousins of Pattern Recognition Receptor Family to Regulate Immune Homeostasis

Kumar,

Stewart

2024

IJMS

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Pattern recognition receptors (PRRs) recognize danger signals such as PAMPs/MAMPs and DAMPs to initiate a protective immune response. TLRs, NLRs, CLRs, and RLRs are well-characterized PRRs of the host immune system. cGLRs have been recently identified as PRRs. In humans, the cGAS/STING signaling pathway is a part of cGLRs. cGAS recognizes cytosolic dsDNA as a PAMP or DAMP to initiate the STING-dependent immune response comprising type 1 IFN release, NF-κB activation, autophagy, and cellular senescence. The present article discusses the emergence of cGLRs as critical PRRs and how they regulate immune responses. We examined the role of cGAS/STING signaling, a well-studied cGLR system, in the activation of the immune system. The following sections discuss the role of cGAS/STING dysregulation in disease and how immune cross-talk with other PRRs maintains immune homeostasis. This understanding will lead to the design of better vaccines and immunotherapeutics for various diseases, including infections, autoimmunity, and cancers.

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Section: Alr and Nlr Interaction With Cgas/sting Signalingmentioning

confidence: 99%

cGLRs Join Their Cousins of Pattern Recognition Receptor Family to Regulate Immune Homeostasis

Kumar,

Stewart

2024

IJMS

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“…NF-κB regulates inflammation through nuclear translocation followed by the expression of pro-inflammatory factors [ 166 ]. H 2 S can modulate the activity of NF-κB activity through trans-sulfonation mechanisms, resulting in the inhibition of the nuclear translocation of NF-κB and a reduced inflammatory response [ 167 , 168 ]. In addition, H 2 S can inhibit the phosphorylation of the p65 NF-κB subunit, preventing the activation of this transcription factor [ 50 ].…”

Section: The Role Of H 2 S In Cell Death In Neurot...mentioning

confidence: 99%

The Role of Hydrogen Sulfide in Regulation of Cell Death following Neurotrauma and Related Neurodegenerative and Psychiatric Diseases

Rodkin

Nwosu

Sannikov

et al. 2023

IJMS

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Injuries of the central (CNS) and peripheral nervous system (PNS) are a serious problem of the modern healthcare system. The situation is complicated by the lack of clinically effective neuroprotective drugs that can protect damaged neurons and glial cells from death. In addition, people who have undergone neurotrauma often develop mental disorders and neurodegenerative diseases that worsen the quality of life up to severe disability and death. Hydrogen sulfide (H2S) is a gaseous signaling molecule that performs various cellular functions in normal and pathological conditions. However, the role of H2S in neurotrauma and mental disorders remains unexplored and sometimes controversial. In this large-scale review study, we examined the various biological effects of H2S associated with survival and cell death in trauma to the brain, spinal cord, and PNS, and the signaling mechanisms underlying the pathogenesis of mental illnesses, such as cognitive impairment, encephalopathy, depression and anxiety disorders, epilepsy and chronic pain. We also studied the role of H2S in the pathogenesis of neurodegenerative diseases: Alzheimer’s disease (AD) and Parkinson’s disease (PD). In addition, we reviewed the current state of the art study of H2S donors as neuroprotectors and the possibility of their therapeutic uses in medicine. Our study showed that H2S has great neuroprotective potential. H2S reduces oxidative stress, lipid peroxidation, and neuroinflammation; inhibits processes associated with apoptosis, autophagy, ferroptosis and pyroptosis; prevents the destruction of the blood-brain barrier; increases the expression of neurotrophic factors; and models the activity of Ca2+ channels in neurotrauma. In addition, H2S activates neuroprotective signaling pathways in psychiatric and neurodegenerative diseases. However, high levels of H2S can cause cytotoxic effects. Thus, the development of H2S-associated neuroprotectors seems to be especially relevant. However, so far, all H2S modulators are at the stage of preclinical trials. Nevertheless, many of them show a high neuroprotective effect in various animal models of neurotrauma and related disorders. Despite the fact that our review is very extensive and detailed, it is well structured right down to the conclusions, which will allow researchers to quickly find the proper information they are interested in.

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“…VSMC function contributes to the formation, growth/development, and even rupture of atherosclerotic plaque [ 20 ]. In the arterial wall, endogenous H 2 S dominant derived from VSMCs [ 70 ]. Numerous evidence, direct and indirect, including in vivo and in vitro studies, demonstrated that the endogenous CSE/H 2 S system may mediate VSMC proliferation, cell death (apoptosis, autophagy, ferroptosis), phage-like differentiation, and calcification, to participate in the pathophysiological process of plaque stability ( Figure 1 ).…”

Section: Cystathionine γ Lyase/hydrogen Sulfide Role In Atherosclerot...mentioning

confidence: 99%

The Role of Hydrogen Sulfide in Plaque Stability

Lin

Geng

2022

Antioxidants

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Atherosclerosis is the greatest contributor to cardiovascular events and is involved in the majority of deaths worldwide. Plaque rapture or erosion precipitates life-threatening thrombi, resulting in the obstruction blood flow to the heart (acute coronary syndrome), brain (ischemic stroke) or low extremities (peripheral vascular diseases). Among these events, major causation dues to the plaque rupture. Although the initiation, procession, and precise time of controlling plaque rupture are unclear, foam cell formation and apoptosis, cell death, extracellular matrix components, protease expression and activity, local inflammation, intraplaque hemorrhage, and calcification contribute to the plaque instability. These alterations tightly associate with the function regulation of intraplaque various cell populations. Hydrogen sulfide (H2S) is gasotransmitter derived from methionine metabolism and exerts a protective role in the genesis of atherosclerosis. Recent progress also showed H2S mediated the plaque stability. In this review, we discuss the progress of endogenous H2S modulation on functions of vascular smooth muscle cells, monocytes/macrophages, and T cells, and the molecular mechanism in plaque stability.

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Hydrogen Sulfide and the Immune System

Cited by 8 publications

References 241 publications

cGLRs Join Their Cousins of Pattern Recognition Receptor Family to Regulate Immune Homeostasis

cGLRs Join Their Cousins of Pattern Recognition Receptor Family to Regulate Immune Homeostasis

The Role of Hydrogen Sulfide in Regulation of Cell Death following Neurotrauma and Related Neurodegenerative and Psychiatric Diseases

The Role of Hydrogen Sulfide in Plaque Stability

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