Hydrogen sulfide primes diabetic wound to close through inhibition of NETosis

Chen, Li; Chen, Wan-ling; Li, Na; Chen, Meiji; Li, Xiang; Zheng, Xue; Zhao, Yue-ze; Wu, Yibo; Xian, Ming; Liu, Jinbao

doi:10.1016/j.mce.2018.10.013

Cited by 69 publications

(65 citation statements)

References 38 publications

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“…The use of H 2 S or the endogenous L-cysteine in vitro blocks the production of IL-8 and monocyte chemoattractant protein-1 (MCP-1) in the human U937 monocyte cell line incubated in high-glucose medium (159). Yang et al have shown that H 2 S treatment decreases NETosis and enhances the healing process of diabetic wounds by preventing ROS-dependent ERK1/2 and p38 activation (161). It has been shown that the levels of NET components, including histones, elastase and proteinase-3, are elevated in the sera from patients with diabetic foot ulcers (162).…”

Section: Neutrophilsmentioning

confidence: 99%

The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System

et al. 2020

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Metabolic abnormalities such as dyslipidemia, hyperinsulinemia, or insulin resistance and obesity play key roles in the induction and progression of type 2 diabetes mellitus (T2DM). The field of immunometabolism implies a bidirectional link between the immune system and metabolism, in which inflammation plays an essential role in the promotion of metabolic abnormalities (e.g., obesity and T2DM), and metabolic factors, in turn, regulate immune cell functions. Obesity as the main inducer of a systemic low-level inflammation is a main susceptibility factor for T2DM. Obesity-related immune cell infiltration, inflammation, and increased oxidative stress promote metabolic impairments in the insulin-sensitive tissues and finally, insulin resistance, organ failure, and premature aging occur. Hyperglycemia and the subsequent inflammation are the main causes of micro-and macroangiopathies in the circulatory system. They also promote the gut microbiota dysbiosis, increased intestinal permeability, and fatty liver disease. The impaired immune system together with metabolic imbalance also increases the susceptibility of patients to several pathogenic agents such as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Thus, the need for a proper immunization protocol among such patients is granted. The focus of the current review is to explore metabolic and immunological abnormalities affecting several organs of T2DM patients and explain the mechanisms, whereby diabetic patients become more susceptible to infectious diseases.

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Section: Neutrophilsmentioning

confidence: 99%

The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System

et al. 2020

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“…Impaired angiogenesis is one of the hallmarks of diabetes which is involved in the pathogenesis of nephropathy, wound and critical limb ischemia in diabetes [ 4 , [117] , [118] , [119] ]. The risk factors involved in diabetes-impaired angiogenesis are suggested to be related to many factors, including hypoxia, chronic inflammation, oxidative stress, hyperglycemia/advanced glycation end products (AGE), connective tissue growth factors, lipoxidation and its products [ 120 ].…”

Section: H 2 S In Diabetes-impaired Angiogenesismentioning

confidence: 99%

“…Angiogenesis is impaired in diabetes [ 4 , 117 ]. However, the underlying mechanisms of diabetes-impaired angiogenesis remain unclear.…”

Section: H 2 S In Diabetes-impaired Angiogenesismentioning

confidence: 99%

Potential role of hydrogen sulfide in diabetes-impaired angiogenesis and ischemic tissue repair

Cheng

2020

Redox Biology

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Diabetes is one of the most prevalent metabolic disorders and is estimated to affect 400 million of 4.4% of population worldwide in the next 20 year. In diabetes, risk to develop vascular diseases is two-to four-fold increased. Ischemic tissue injury, such as refractory wounds and critical ischemic limb (CLI) are major ischemic vascular complications in diabetic patients where oxygen supplement is insufficient due to impaired angiogenesis/neovascularization. In spite of intensive studies, the underlying mechanisms of diabetes-impaired ischemic tissue injury remain incompletely understood. Hydrogen sulfide (H 2 S) has been considered as a third gasotransmitter regulating angiogenesis under physiological and ischemic conditions. Here, the underlying mechanisms of insufficient H 2 S-impaired angiogenesis and ischemic tissue repair in diabetes are discussed. We will primarily focuses on the signaling pathways of H 2 S in controlling endothelial function/biology, angiogenesis and ischemic tissue repair in diabetic animal models. We summarized that H 2 S plays an important role in maintaining endothelial function/biology and angiogenic property in diabetes. We demonstrated that exogenous H 2 S may be a theraputic agent for endothelial dysfunction and impaired ischemic tissue repair in diabetes.

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“…Na 2 S promotes wound healing by reducing NETs and NETosis levels, which might be due to ROS suppression followed by ERK1/2 and p38 phosphorylation inhibition in a NETosis model of neutrophils induced by phorbol 12-myristate 13-acetate (PMA) ( Fig. 1 ) [37] . Another study also confirmed that both NaHS and 4-hydro-xythiobenzamide promote wound healing in db/db diabetic mice [38] .…”

Section: Implications Of Hydrogen Sulfide In Dermatologymentioning

confidence: 99%

Hydrogen sulfide: Recent progress and perspectives for the treatment of dermatological diseases

Zhang

Shen

et al. 2021

Journal of Advanced Research

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Hydrogen sulfide primes diabetic wound to close through inhibition of NETosis

Cited by 69 publications

References 38 publications

The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System

The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System

Potential role of hydrogen sulfide in diabetes-impaired angiogenesis and ischemic tissue repair

Hydrogen sulfide: Recent progress and perspectives for the treatment of dermatological diseases

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