When apoptosis meets autophagy: deciding cell fate after trauma and sepsis

Hsieh, Ya‐Ching; Athar, Mohammad; Chaudry, Irshad H.

doi:10.1016/j.molmed.2009.01.002

Cited by 107 publications

(91 citation statements)

References 90 publications

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“…5,29,40 However, numerous studies have indicated autophagy suppression at the late stage of the disease. The reduced autophagy activity is associated with organ failure.…”

Section: Discussionmentioning

confidence: 99%

“…39 Autophagy and apoptosis also share common molecular regulators and appear to be antagonistic. 40 To this end, inhibition of autophagy by interferon regulatory factor IRF1 has been shown to activates apoptosis in splenic macrophages. 30 Physiologically, exhaustion of autophagy may result in extrusion of accumulated autophagosomes out of the cells, leading to a proinflammatory response.…”

Section: Kinetics Of Autophagy In Sepsismentioning

confidence: 99%

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Autophagy in sepsis: Degradation into exhaustion?

Wong

et al. 2016

Autophagy

126

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Autophagy is one of the innate immune defense mechanisms against microbial challenges. Previous in vitro and in vivo models of sepsis demonstrated that autophagy was activated initially in sepsis, followed by a subsequent phase of impairment. Autophagy modulation appears to be protective against multiple organ injuries in these murine sepsis models. This is achieved in part by preventing apoptosis, maintaining a balance between the productions of pro-and anti-inflammatory cytokines, and preserving mitochondrial functions. This article aims to discuss the role of autophagy in sepsis and the therapeutic potential of autophagy enhancers.

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“…5,29,40 However, numerous studies have indicated autophagy suppression at the late stage of the disease. The reduced autophagy activity is associated with organ failure.…”

Section: Discussionmentioning

confidence: 99%

Section: Kinetics Of Autophagy In Sepsismentioning

confidence: 99%

Autophagy in sepsis: Degradation into exhaustion?

Wong

et al. 2016

Autophagy

126

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“…The 'choice' between autophagy and apoptosis may be integral to the fate of cells. The reciprocal regulation between apoptosis and autophagy may affect immune homeostasis in sepsis (28). The induction of autophagy may re-engage or preserve host immune homeostasis, and may avoid the side effects of complete inhibition of apoptosis (28).…”

Section: Clinical Application: Restoration Of Immune Homeostasis By Amentioning

confidence: 99%

“…It has been demonstrated that mitochondria may undergo autophagy, which may be detrimental for the switch between autophagy and apoptosis (28). The term mitophagy is used to refer to mitochondrial degradation by autophagy.…”

Section: Reciprocal Regulation Between Apoptosis and Autophagymentioning

confidence: 99%

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Clinical application: Restoration of immune homeostasis by autophagy as a potential therapeutic target in sepsis

Zhang

Tsung

2016

Experimental and Therapeutic Medicine

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Abstract. Sepsis-induced lymphocyte and dendritic cell apoptosis contributes to immunosuppression, resulting in an inability to eradicate the primary infection and a propensity to acquire secondary infections. However, the inhibition of apoptosis may produce unexpected and undesirable consequences. Another cellular process, autophagy, is also activated in immune cells. There is increasing evidence to suggest that autophagy confers a protective effect in sepsis. The protective mechanisms underlying this effect include limiting apoptotic cell death and maintaining cellular homeostasis. Therefore, understanding the regulation of immune cell autophagy and apoptosis may provide insight into novel therapeutic strategies. The present review examined potential novel therapeutic strategies aimed at restoring immune homeostasis by inducing autophagy. The restoration of balance between apoptosis and autophagy may be a novel approach for improving sepsis-induced immunosuppression and decreasing susceptibility to sepsis. Contents1. Introduction 2. Immune cell apoptosis in sepsis 3. Immune cell autophagy in sepsis 4. Regulation immunity and inflammation 5. Reciprocal regulation between apoptosis and autophagy 6. Autophagy as a therapeutic target in pulmonary diseases 7. Autophagy as a potential therapeutic target for sepsis 8. Conclusion IntroductionDespite major advances in critical care management and antibiotic therapies, sepsis-induced multiple organ failure (MOF) continues to contribute to significant morbidity and mortality in intensive care units (ICUs) (1). MOF is the second leading cause of death among patients in non-coronary ICUs, and the tenth leading cause of death in the United States (2). In the United States, an estimated 250,000 individuals succumb to sepsis every year. The incidence of sepsis is increasing at a rate of 1.5% per annum and mortality rates of ≤70% have been estimated (3). Furthermore, this mortality rate has remained essentially unchanged for the past 25 years (2,4).Treating patients with severe sepsis and septic shock has been a great challenge. This is due to the incomplete understanding of the complex biological processes underlying sepsis, which has hindered the development of sepsis-specific therapies (1). Thus, it is essential to determine the mechanism underlying the pathophysiology of sepsis so that more effective therapeutic strategies may be developed.Traditionally, sepsis has been considered to be an overwhelming inflammatory response, which results in MOF from which the patient ultimately succumbs (1). However, over the past 25 years, numerous clinical trials involving agents that block the inflammatory cascade, such as anti-endotoxin antibodies (5), interleukin-1 (IL-1) receptor antagonists (6), and tumor necrosis factor-α (TNF-α) antagonists (7), have failed to improve the outcome of sepsis. The failure of anti-inflammatory agents highlights the fact that further research is required in order to elucidate the mechanisms underlying the septic response.Numerous mechanisms underlie s...

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Berberine: A novel therapeutic strategy for cancer

et al. 2020

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Cancer, even currently, is one of the main reasons for mortality and morbidity, worldwide. In recent years, a great deal of effort has been made to find efficient therapeutic strategies for cancer, however, particularly with regards to side effects and the possibility of complete remission. Berberine (BBR) is a nature‐driven phytochemical component originated from different plant groups such as Berberis vulgaris, Berberis aquifolium, and Berberis aristata. BBR is a well‐known nutraceutical because of its wide range of pharmacological activities including anti‐inflammatory, antidiabetic, antibacterial, antiparasitic, antidiarrheal, antihypertensive, hypolipidemic, and fungicide. In addition, it exhibits inhibitory effects on multiple types of cancers. In this review, we have elaborated on the anticancer effects of BBR through the regulation of different molecular pathways such as: inducing apoptosis, autophagy, arresting cell cycle, and inhibiting metastasis and invasion.

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When apoptosis meets autophagy: deciding cell fate after trauma and sepsis

Cited by 107 publications

References 90 publications

Autophagy in sepsis: Degradation into exhaustion?

Autophagy in sepsis: Degradation into exhaustion?

Clinical application: Restoration of immune homeostasis by autophagy as a potential therapeutic target in sepsis

Berberine: A novel therapeutic strategy for cancer

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