Impact of insulin on the intestinal microcirculation in a model of sepsis-related hyperglycemia

Caldwell, Alexa; Morick, Jan Niklas; Jentsch, Anne-Marie; Wegner, Annette; Pavlović, Dragan; Al-Banna, Nadia; Lehmann, Christian

doi:10.1016/j.mvr.2018.05.004

Cited by 5 publications

(3 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the vascular endothelium, an imbalance between inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) may play a certain role in sepsis microcirculation dysfunction. [4] The integrity of the vascular endothelial glycocalyx plays a key role in the intestinal microcirculation, which can inhibit intercellular adhesion. [5] Glycocalyx degradation can occur in certain pathologic conditions, such as septic shock.…”

Section: Endothelial Dysfunctionmentioning

confidence: 99%

“…Insulin administration improves intestinal microcirculation and reduces leukocyte activation in septic rats through immune regulation, vascular regulation and regulation of the prostaglandin A2 (PGA2)/thromboxane A2 (TxA2) balance of insulin. [4] The new iron chelator DIBI can inhibit iron-catalyzed ROS production, thereby improving microcirculation. [40] Deletion of cIAP2 showed potential therapeutic benefit in endotoxemia.…”

Section: Other Treatmentsmentioning

confidence: 99%

See 1 more Smart Citation

Intestinal microcirculation dysfunction in sepsis: pathophysiology, clinical monitoring, and therapeutic interventions

Tang¹

2022

World J Emerg Med

View full text Add to dashboard Cite

BACKGROUND: Intestinal microcirculation dysfunction is an important factor that causes poor prognosis in sepsis patients and is an important pathophysiological basis for the occurrence and development of sepsis.DATA RESOURCES: PubMed, Web of Science, and China National Knowledge Infrastructure (CNKI) were searched from inception to August 1, 2021. The search was limited to the English language only. Two reviewers independently identified studies related to intestinal microcirculation dysfunction in sepsis. Exclusion criteria were duplicate articles according to multiple search criteria.RESULTS: Fifty articles were included, and most of them were animal studies. These studies reported pathogenesis, including endothelial dysfunction, leukocyte recruitment and adhesion, microthrombus formation, microcirculation hypoperfusion, and redistribution of intestinal wall blood flow. The monitoring methods of intestinal microcirculation were also diverse, including handheld microscopes, intravital microscopy (IVM), laser Doppler blood flow instruments, laser speckle contrast imaging, tissue refl ectance spectrophotometry, biochemical markers of intestinal ischemia, and histopathological examination. In view of the related pathogenesis of intestinal microcirculation disorder in sepsis, existing studies also have diff erent opinions on its treatment.CONCLUSIONS: Limited by monitoring, there are few clinical studies on intestinal microcirculation dysfunction in sepsis. Related research mainly focuses on basic research, but some progress has also been made. Therefore, this review may provide a reference for future research on intestinal microcirculation dysfunction in sepsis.

show abstract

Section: Endothelial Dysfunctionmentioning

confidence: 99%

Section: Other Treatmentsmentioning

confidence: 99%

Intestinal microcirculation dysfunction in sepsis: pathophysiology, clinical monitoring, and therapeutic interventions

Tang¹

2022

World J Emerg Med

View full text Add to dashboard Cite

show abstract

“…Extracellular SQSTM1 also acts as a new proinflammatory mediator through its binding to the insulin receptor (INSR), leading to a nuclear factor kappa B (NFKB)dependent metabolic switch towards aerobic glycolysis, followed by proinflammatory 'M1' polarization of macrophages (Figure 3) [78]. Unlike the insulin-INSR axis [79], the SQSTM1-INSR axis-mediated NFKB activation and inflammatory response occurs in macrophages through a pathway that requires PLCG1-dependent lipid peroxidation [78] and subsequent elevated pyroptosis [80]. Based on western blot assays, conditional depletion of glutathione peroxidase 4 (GPX4, which reduces hydrogen peroxide, organic hydroperoxides, and lipid peroxides) in mouse myeloid cells (LysM-Cre;Gpx4 f/f ) increases the activity of PLCG1 to induce pyroptosis [80].…”

Section: Hmgb1mentioning

confidence: 99%