Cortistatin protects myocardium from endoplasmic reticulum stress induced apoptosis during sepsis

Zhang, Bo; Liu, Yue; Zhang, Jinsheng; Zhang, Xiaohui; Chen, Wen-Jia; Yin, Xinhua; Qi, Yongfen

doi:10.1016/j.mce.2015.02.016

Cited by 54 publications

(42 citation statements)

References 30 publications

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“…Interestingly, attenuation of ER stress with pharmacological or gene therapy strategies has been successful in reducing pathological features in various experimental models of inflammatory diseases [14, 24, 27, 28]. Thus, we demonstrate that investigation on ER stress will hold promise to reveal novel therapeutic targets for the inflammatory diseases including sepsis in human.…”

Section: Introductionmentioning

confidence: 72%

“…There is growing interest in investigating the regulatory mechanisms underlying ER stress and UPR signaling and the development of strategies to target this pathway, since there is substantial evidences for the participation of ER stress in many diseases, including inflammatory disorders, neurodegeneration, cancer, and diabetes [18, 24-26]. Interestingly, attenuation of ER stress with pharmacological or gene therapy strategies has been successful in reducing pathological features in various experimental models of inflammatory diseases [14, 24, 27, 28].…”

Section: Introductionmentioning

confidence: 99%

“…Myocardial depression is a well-recognized manifestation of organ dysfunction in sepsis, and myocardial apoptosis is a key step for this progression. A very recent study reported that components of ER stress (GRP94, CHOP, and caspase-12) were up regulated in the hearts of septic rats and inhibition of ER stress protected the myocardial from ER stress induced apoptosis in rats [24]. CHOP/GADD153 (growth arrest/DNA damage) plays a convergent role in the UPR and has been identified as one of the most important mediators of ER stress-induced apoptosis [29, 30, 89, 90].…”

Section: Introductionmentioning

confidence: 99%

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Endoplasmic Reticulum Stress in Sepsis

Khan

Yang

Wang

2015

Shock

109

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Sepsis is an enormous public health issue and the leading cause of death in critically ill patients in intensive care units (ICU). Overwhelming inflammation, characterized by cytokine storm, oxidative threats, and neutrophil sequestration is an underlying component of sepsis-associated organ failure. Despite recent advances in sepsis research, there is still no effective treatment available beyond the standard of care and supportive therapy. To reduce sepsis-related mortality, a better understanding of the biological mechanism associated with the sepsis is essential. Endoplasmic reticulum (ER), a subcellular organelle is responsible for the facilitation of protein folding and assembly and involved in several other physiological activities. Under the stress and inflammation condition, ER loses the homeostasis in its function, which is termed as ER stress. During ER stress, unfolded protein response (UPR) is activated to restore ER function to its normal balance. However, once the stress is beyond the compensatory capacity of UPR or protracted, the apoptosis would be initiated by triggering cell injuries, even to cell death. As such, ER stress and UPR are reported to be implicated in several pathological and inflammatory conditions. Although the detrimental role of ER stress during infections has been demonstrated, there is growing evidences that ER stress participate in the pathogenesis of sepsis. In this review, we summarize the current research in the context of ER stress and UPR signaling associated with sepsis and its related clinical conditions, such as trauma- hemorrhage, and ischemia/reperfusion (I/R) injury. We also discuss the potential implication of ER stress as a novel therapeutic target and prognostic marker in patients with sepsis.

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Section: Introductionmentioning

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Endoplasmic Reticulum Stress in Sepsis

Khan

Yang

Wang

2015

Shock

109

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“…reported that heat stress induced the mRNA and protein expression of BAX in LLC-PK1 cells, significantly increasing the ratio of Bcl-2 and BAX48. Other studies reported that knockout IP3R1 in T Jurkat lymphocytes prevented apoptosis49 and that apoptosis can also be prevented by blocking the SERCA1 protein50.…”

Section: Discussionmentioning

confidence: 99%

“…Zhang et al 48. reported that heat stress induced the mRNA and protein expression of BAX in LLC-PK1 cells, significantly increasing the ratio of Bcl-2 and BAX48.…”

Section: Discussionmentioning

confidence: 99%

Elucidating a molecular mechanism that the deterioration of porcine meat quality responds to increased cortisol based on transcriptome sequencing

Wan

Wang

Xiong

et al. 2016

Sci Rep

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Stress response is tightly linked to meat quality. The current understanding of the intrinsic mechanism of meat deterioration under stress is limited. Here, male piglets were randomly assigned to cortisol and control groups. Our results showed that when serum cortisol level was significantly increased, the meat color at 1 h postmortem, muscle bundle ratio, apoptosis rate, and gene expression levels of calcium channel and cell apoptosis including SERCA1, IP3R1, BAX, Bcl-2, and Caspase-3, were notably increased. However, the value of drip loss at 24 h postmortem and serum CK were significantly decreased. Additionally, a large number of differentially expressed genes (DEGs) in GC regulation mechanism were screened out using transcriptome sequencing technology. A total of 223 DEGs were found, including 80 up-regulated genes and 143 down-regulated genes. A total of 204 genes were enriched in GO terms, and 140 genes annotated into in KEGG database. Numerous genes were primarily involved in defense, inflammatory and wound responses. This study not only identifies important genes and signalling pathways that may affect the meat quality but also offers a reference for breeding and feeding management to provide consumers with better quality pork products.

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The role of lncRNA MALAT1 in cardiovascular disease

Yan

Song

et al. 2019

IUBMB Life

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Cardiovascular disease (CVD) is the first leading cause of death worldwide. Understanding the molecular mechanism of signaling pathways involved in pathology of CVD is benefit for targeted therapeutics. Recently, long non‐coding RNAs (lncRNAs) are found and involved in regulation of pathology of CVD at different levels. Among them, MALAT1 attracted more attention as it was profoundly expressed in endothelial cells or cardiomyocytes in response to the risk factors of CVD, such as hypoxia, high glucose, cytokine, and oxidative stress. In this review, we summarize recent progresses in research on the molecular mechanism of MALAT1 on regulating the pathophysiological processes of CVD as well as its potential therapeutic applications.

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Cortistatin protects myocardium from endoplasmic reticulum stress induced apoptosis during sepsis

Cited by 54 publications

References 30 publications

Endoplasmic Reticulum Stress in Sepsis

Endoplasmic Reticulum Stress in Sepsis

Elucidating a molecular mechanism that the deterioration of porcine meat quality responds to increased cortisol based on transcriptome sequencing

The role of lncRNA MALAT1 in cardiovascular disease

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