Palmitate reduces starvation-induced ER stress by inhibiting ER-phagy in hypothalamic cells

Lim, Yean Teng; Kim, Seolsong; Kim, Eunkyoung

doi:10.1186/s13041-021-00777-8

Cited by 11 publications

(2 citation statements)

References 68 publications

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“…Regarding other types of autophagy that could be affected by TFEB activation, the flux of autophagy or ER-phagy was not increased by HFD feeding despite TFEB activation in pancreatic islets 70 . These results are consistent with previous papers reporting no increase in autophagy or ER-phagy flux by PA or HFD feeding 77 , 91 , 92 and could be attributable to distinct molecular machinery that is required for the autophagic removal of different organelles.…”

Section: Functional Role Of Tfeb-mediated Mitophagy Under Conditions ...supporting

confidence: 93%

Pancreatic β-cell mitophagy as an adaptive response to metabolic stress and the underlying mechanism that involves lysosomal Ca2+ release

Oh,

Park,

Sonn

et al. 2023

Exp Mol Med

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Mitophagy is an excellent example of selective autophagy that eliminates damaged or dysfunctional mitochondria, and it is crucial for the maintenance of mitochondrial integrity and function. The critical roles of autophagy in pancreatic β-cell structure and function have been clearly shown. Furthermore, morphological abnormalities and decreased function of mitochondria have been observed in autophagy-deficient β-cells, suggesting the importance of β-cell mitophagy. However, the role of authentic mitophagy in β-cell function has not been clearly demonstrated, as mice with pancreatic β-cell-specific disruption of Parkin, one of the most important players in mitophagy, did not exhibit apparent abnormalities in β-cell function or glucose homeostasis. Instead, the role of mitophagy in pancreatic β-cells has been investigated using β-cell-specific Tfeb-knockout mice (TfebΔβ-cell mice); Tfeb is a master regulator of lysosomal biogenesis or autophagy gene expression and participates in mitophagy. TfebΔβ-cell mice were unable to adaptively increase mitophagy or mitochondrial complex activity in response to high-fat diet (HFD)-induced metabolic stress. Consequently, TfebΔβ-cell mice exhibited impaired β-cell responses and further exacerbated metabolic deterioration after HFD feeding. TFEB was activated by mitochondrial or metabolic stress-induced lysosomal Ca2+ release, which led to calcineurin activation and mitophagy. After lysosomal Ca2+ release, depleted lysosomal Ca2+ stores were replenished by ER Ca2+ through ER→lysosomal Ca2+ refilling, which supplemented the low lysosomal Ca2+ capacity. The importance of mitophagy in β-cell function was also demonstrated in mice that developed β-cell dysfunction and glucose intolerance after treatment with a calcineurin inhibitor that hampered TFEB activation and mitophagy.

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Section: Functional Role Of Tfeb-mediated Mitophagy Under Conditions ...supporting

confidence: 93%

Pancreatic β-cell mitophagy as an adaptive response to metabolic stress and the underlying mechanism that involves lysosomal Ca2+ release

Oh,

Park,

Sonn

et al. 2023

Exp Mol Med

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“…Liu and colleagues found that Dexmedetomidine induces ER-phagy by activating FAM134B, which subsequently attenuated the ER stress (75). Globular adiponectin has been found to activate SEC62mediated ER-phagy, thus mitigating ER stress-induced cardiomyocytes apoptosis (76).However, Lim et al found that palmitate reduces ER stress by inhibiting ER-phagy (77). Persistent ER stress has been demonstrated to cause apoptosis of alveolar epithelial cells, whereas appropriate ER-phagy decreases apoptosis by alleviating ER stress.…”

Section: Er-phagy Inhibits the Apoptosis Of Alveolar Epithelial Cells...mentioning

confidence: 99%

Role of endoplasmic reticulum autophagy in acute lung injury

et al. 2023

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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), the prime causes of morbidity and mortality in critically ill patients, are usually treated by general supportive treatments. Endoplasmic reticulum autophagy (ER-phagy) maintains cellular homeostasis by degrading damaged endoplasmic reticulum (ER) fragments and misfolded proteins. ER-phagy is crucial for maintaining ER homeostasis and improving the internal environment. ER-phagy has a particular role in some aspects, such as immunity, inflammation, cell death, pathogen infection, and collagen quality. In this review, we summarized the definition, epidemiology, and pathophysiology of ALI/ARDS and described the regulatory mechanisms and functions of ER-phagy as well as discussed the potential role of ER-phagy in ALI/ARDS from the perspectives of immunity, inflammation, apoptosis, pathogen infection, and fibrosis to provide a novel and effective target for improving the prognosis of ALI/ARDS.

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Regulation of genes involved in the metabolic adaptation of murine microglial cells in response to elevated HIF-1α mediated activation

Florance,

Ramasubbu

2024

Immunogenetics

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Palmitate reduces starvation-induced ER stress by inhibiting ER-phagy in hypothalamic cells

Cited by 11 publications

References 68 publications

Pancreatic β-cell mitophagy as an adaptive response to metabolic stress and the underlying mechanism that involves lysosomal Ca2+ release

Pancreatic β-cell mitophagy as an adaptive response to metabolic stress and the underlying mechanism that involves lysosomal Ca2+ release

Role of endoplasmic reticulum autophagy in acute lung injury

Regulation of genes involved in the metabolic adaptation of murine microglial cells in response to elevated HIF-1α mediated activation

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