Ischemic brain injury in diabetes and endoplasmic reticulum stress

Rehni, Ashish K.; Cho, Sunjoo

doi:10.1016/j.neuint.2021.105219

Cited by 8 publications

(4 citation statements)

References 168 publications

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“…In addition, ROS can lead to mitochondrial and endoplasmic reticulum disruption, facilitating the release of cytochrome c (such as a pro-apoptotic protein) and additional Ca 2 ions in the cytosol. This phenomenon determines ischemic insult amplification and apoptosis [ 16 , 17 ].…”

Section: An Overview Of the Pathogenesis Of Cerebral Ischemiamentioning

confidence: 99%

“…The pathways NF-κB and MAPK partially induce the expression and activation of NLRP1 and NLRP3 inflammatory proteins in vivo and in vitro under ischemic conditions [ 34 ]. Reports show that ischemic stroke increases the expression and activation of NLRP3 inflammatory proteins in glial cells and neurons [ 17 ].…”

Section: An Overview Of the Pathogenesis Of Cerebral Ischemiamentioning

confidence: 99%

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Molecular Mechanisms of Inflammasome in Ischemic Stroke Pathogenesis

et al. 2022

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Ischemic stroke (also called cerebral ischemia) is one of the leading causes of death and severe disability worldwide. NLR inflammasomes play a crucial role in sensing cell damage in response to a harmful stimuli and modulating the inflammatory response, promoting the release of pro-inflammatory cytokines such as IL-18 and IL-1β following ischemic injury. Therefore, a neuroprotective effect is achieved by inhibiting the expression, assembly, and secretion of inflammasomes, thus limiting the extent of brain detriment and neurological sequelae. This review aims to illustrate the molecular characteristics, expression levels, and assembly of NLRP3 (nucleotide-binding oligomerization domain-like receptor [NLR] family pyrin-domain-containing 3) inflammasome, the most studied in the literature, in order to discover promising therapeutic implications. In addition, we provide some information regarding the contribution of NLRP1, NLRP2, and NLRC4 inflammasomes to ischemic stroke pathogenesis, highlighting potential therapeutic strategies that require further study.

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Section: An Overview Of the Pathogenesis Of Cerebral Ischemiamentioning

confidence: 99%

Section: An Overview Of the Pathogenesis Of Cerebral Ischemiamentioning

confidence: 99%

Molecular Mechanisms of Inflammasome in Ischemic Stroke Pathogenesis

et al. 2022

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“…6,7 The endoplasmic reticulum is an important to maintain cellular homeostasis. 8 Accumulating evidence has pointed out that ER tress contributes to degeneration and neuronal dysfunction of the central nervous system, such as brain injury 9 and SCI. 10 After SCI, excessive ER tress initiates an overstressed unfolded protein response, eventually leading to neuronal apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Sitagliptin attenuates neuronal apoptosis via inhibiting the endoplasmic reticulum stress after acute spinal cord injury

Tang

Dai

et al. 2023

Hum Exp Toxicol

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Regulation of endoplasmic reticulum stress (ER) stress-induced apoptosis and nerve regeneration is a hopeful way for acute spinal cord injury (SCI). Sitagliptin (Sita) is one of dipeptidyl peptidase-4 (DPP-4) inhibitor, which is beneficial neurons damaged diseases. However, its protective mechanisms of avoiding nerve injury remain unclear. In this study, we further investigated the mechanism of the anti-apoptotic and neuroprotective effects of Sita in promoting locomotor recovery from SCI. In vivo results showed that Sita treatment reduced neural apoptosis caused by SCI. Moreover, Sita effectively attenuated the ER tress and associated apoptosis in rats with SCI. A striking feature was the occurrence of nerve fiber regeneration at the lesion site, which eventually led to significant locomotion recovery. In vitro results showed that the PC12 cell injury model induced by Thapsigargin (TG) also showed similar neuroprotective effects. Overall, sitagliptin showed potent neuroprotective effects by targeting the ER stress-induced apoptosis both in vivo and vitro, thus facilitating the regeneration of the injured spinal cord.

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“…IR, which is present in the majority of type II diabetes (T2D) patients, promotes the development of ischemic stroke and is associated with a poor prognosis ( 4 , 5 ). One of the best-known effects of IR is the presence of hyperglycemia, which may negatively affect brain function through various mechanisms ( 6 ). This review evaluates studies on IR as an independent risk factor for ischemic stroke, with a particular focus on the mechanisms and therapy associated with IR and ischemic stroke.…”

Section: Introductionmentioning

confidence: 99%

Insulin resistance in ischemic stroke: Mechanisms and therapeutic approaches

et al. 2022

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The pathological condition of insulin resistance prevents the neuroprotective effects of insulin. Numerous studies have demonstrated that insulin resistance, as an independent risk factor for ischemic stroke, accelerates the formation of thrombosis and promotes the development of atherosclerosis, both of which are major mechanisms of ischemic stroke. Additionally, insulin resistance negatively affects the prognosis of patients with ischemic stroke regardless of whether the patient has diabetes, but the mechanisms are not well studied. We explored the association between insulin resistance and the primary mechanisms of brain injury in ischemic stroke (inflammation, oxidative stress, and neuronal damage), looking for potential causes of poor prognosis in patients with ischemic stroke due to insulin resistance. Furthermore, we summarize insulin resistance therapeutic approaches to propose new therapeutic directions for clinically improving prognosis in patients with ischemic stroke.

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Ischemic brain injury in diabetes and endoplasmic reticulum stress

Cited by 8 publications

References 168 publications

Molecular Mechanisms of Inflammasome in Ischemic Stroke Pathogenesis

Molecular Mechanisms of Inflammasome in Ischemic Stroke Pathogenesis

Sitagliptin attenuates neuronal apoptosis via inhibiting the endoplasmic reticulum stress after acute spinal cord injury

Insulin resistance in ischemic stroke: Mechanisms and therapeutic approaches

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