Polyamines reverse immune senescence via the translational control of autophagy

Zhang, Hanlin; Simon, Anna Katharina

doi:10.1080/15548627.2019.1687967

Cited by 29 publications

(17 citation statements)

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“…In the same way, mice treated with spermidine exhibit prolonged lifespan and improved cardiomyocyte function due to increased cardiac autophagic flux ( Eisenberg et al, 2016 ). Furthermore, it has been recently observed that hypusinated EIF5A controls the synthesis of the transcription factor EB, a master regulator of genes encoding mediators of autophagy, in naive B cells ( Zhang and Simon, 2020 ). This transcription factor was not evidenced to be regulated by infection and/or inhibition of DHPS in our study, suggesting that EIF5A Hyp may regulate autophagy by various pathways.…”

Section: Discussionmentioning

confidence: 99%

Hypusination Orchestrates the Antimicrobial Response of Macrophages

et al. 2020

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Section: Discussionmentioning

confidence: 99%

Hypusination Orchestrates the Antimicrobial Response of Macrophages

et al. 2020

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“…Spermidine, a natural polyamine that promotes autophagy‐dependent longevity (Madeo et al, 2019; Zhang & Simon, 2020), has been shown to promote osteogenic differentiation (Lee et al, 2013) and prevent OVX‐induced bone loss by reducing OC formation and maturation (Yamada et al, 2019; Yamamoto et al, 2012). Lithium is commonly seen as a mood‐stabilizing drug and has recently been thought to induce autophagy by acting on intracellular inositol and inositol‐1,4,5‐triphosphate levels (Motoi et al, 2014; Sarkar et al, 2005).…”

Section: Therapeutic Potential Of Autophagy In Bone Diseasementioning

confidence: 99%

The role of autophagy in bone homeostasis

Guo

Yang

et al. 2021

Journal Cellular Physiology

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Autophagy is an evolutionarily conserved intracellular process and is considered one of the main catabolism pathways. In the process of autophagy, cells are digested nonselectively or selectively to recover nutrients and energy, so it is regarded as an antiaging process. In addition to the essential role of autophagy in cellular homeostasis, autophagy is a stress response mechanism for cell survival. Here, we review recent literature describing the pathway of autophagy and its role in different bone cell types, including osteoblasts, osteoclasts, and osteocytes. Also discussed is the mechanism of autophagy in bone diseases associated with bone homeostasis, including osteoporosis and Paget's disease. Finally, we discuss the application of autophagy regulators in bone diseases. This review aims to introduce autophagy, summarize the understanding of its relevance in bone physiology, and discuss its role and therapeutic potential in the pathogenesis of bone diseases such as osteoporosis.

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“…Interestingly, B cell responses to different stimuli produce different cellular responses fluctuating between canonical to non-canonical autophagy (116,150). Recently, autophagy inducers were able to restore survival of B cells in aging patients with impaired autophagy (151). Changes in autophagic flux and mechanisms make the characterization of B cell autophagy complicated.…”

Section: Ilc2mentioning

confidence: 99%

Role of Autophagy in Lung Inflammation

2020

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Autophagy is a cellular recycling system found in almost all types of eukaryotic organisms. The system is made up of a variety of proteins which function to deliver intracellular cargo to lysosomes for formation of autophagosomes in which the contents are degraded. The maintenance of cellular homeostasis is key in the survival and function of a variety of human cell populations. The interconnection between metabolism and autophagy is extensive, therefore it has a role in a variety of different cell functions. The disruption or dysfunction of autophagy in these cell types have been implicated in the development of a variety of inflammatory diseases including asthma. The role of autophagy in non-immune and immune cells both lead to the pathogenesis of lung inflammation. Autophagy in pulmonary non-immune cells leads to tissue remodeling which can develop into chronic asthma cases with long term effects. The role autophagy in the lymphoid and myeloid lineages in the pathology of asthma differ in their functions. Impaired autophagy in lymphoid populations have been shown, in general, to decrease inflammation in both asthma and inflammatory disease models. Many lymphoid cells rely on autophagy for effector function and maintained inflammation. In stark contrast, autophagy deficient antigen presenting cells have been shown to have an activated inflammasome. This is largely characterized by a T H 17 response that is accompanied with a much worse prognosis including granulocyte mediated inflammation and steroid resistance. The cell specificity associated with changes in autophagic flux complicates its targeting for amelioration of asthmatic symptoms. Differing asthmatic phenotypes between T H 2 and T H 17 mediated disease may require different autophagic modulations. Therefore, treatments call for a more cell specific and personalized approach when looking at chronic asthma cases. Viral-induced lung inflammation, such as that caused by SARS-CoV-2, also may involve autophagic modulation leading to inflammation mediated by lung resident cells. In this review, we will be discussing the role of autophagy in non-immune cells, myeloid cells, and lymphoid cells for their implications into lung inflammation and asthma. Finally, we will discuss autophagy's role viral pathogenesis, immunometabolism, and asthma with insights into autophagic modulators for amelioration of lung inflammation.

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Polyamines reverse immune senescence via the translational control of autophagy

Cited by 29 publications

References 1 publication

Hypusination Orchestrates the Antimicrobial Response of Macrophages

Hypusination Orchestrates the Antimicrobial Response of Macrophages

The role of autophagy in bone homeostasis

Role of Autophagy in Lung Inflammation

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