LncRNA MEG3 regulates autophagy and pyroptosis via FOXO1 in pancreatic β-cells

Li, Xiudan; Bai, Chun-Ying; Wang, Hongjie; Wan, Tingting; Li, Yanbo

doi:10.1016/j.cellsig.2022.110247

Cited by 11 publications

(6 citation statements)

References 38 publications

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“…51,52 It was discovered that certain circRNAs could control protein mRNA binding by acting as molecular sponges and that circRNAs may be better than lncRNAs as biomarkers for their higher stability. ncRNAs do not encode proteins but participate in several pathological processes, such as apoptosis, [52][53][54] pyroptosis, 55,56 and cell proliferation. 54,57 Moreover, abnormal levels of ncRNAs are common in different conditions, including tumors, diabetes, and DR. [58][59][60] 3.2 | The role of ncRNAs in diabetes and VCD ncRNAs are good diagnostic and prognostic biomarkers for a variety of diseases, including metabolic diseases.…”

Section: Ncrnasmentioning

confidence: 99%

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The role of ncRNAs‐mediated pyroptosis in diabetes and its vascular complications

Feng,

Yang,

Zhong

et al. 2024

Cell Biochemistry & Function

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Over the past decade, the prevalence of diabetes has increased significantly worldwide, leading to an increase in vascular complications of diabetes (VCD), such as diabetic cardiomyopathy (DCM), diabetic nephropathy (DN), and diabetic retinopathy (DR). Noncoding RNAs (ncRNAs), such as microRNAs (miRNAs), long Noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), play a key role in cellular processes, including the pathophysiology of diabetes and VCD via pyroptosis. ncRNAs (e.g., miR‐17, lnc‐MEG3, and lnc‐KCNQ1OT1) can regulate pyroptosis in pancreatic β cells. Some ncRNAs are involved in VCD progression. For example, miR‐21, lnc‐KCNQ1OT1, lnc‐GAS5, and lnc‐MALAT1 were reported in DN and DCM, and lnc‐MIAT was identified in DCM and DR. Herein, this review aimed to summarize recent research findings related to ncRNAs‐mediated pyroptosis at the onset and progression of diabetes and VCD.

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Section: Ncrnasmentioning

confidence: 99%

“…ncRNAs do not encode proteins but participate in several pathological processes, such as apoptosis, 52–54 pyroptosis, 55,56 and cell proliferation 54,57 . Moreover, abnormal levels of ncRNAs are common in different conditions, including tumors, diabetes, and DR 58–60 …”

Section: The Role Of Ncrnas In Diabetes and Vcdmentioning

confidence: 99%

The role of ncRNAs‐mediated pyroptosis in diabetes and its vascular complications

Feng,

Yang,

Zhong

et al. 2024

Cell Biochemistry & Function

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“…Previous studies indicate that FoxO1 is also important for pancreatic β cell survival and insulin secretion, e.g., via autophagy (reviewed in [ 159 , 160 ]). In a recent study, FoxO1 silencing in INS-1 cells led to impaired autophagy and reduced cell viability [ 161 ]. Some hypoglycemic drugs, including GLP-1 receptor agonists and GLP-1 analogs, have been reported to stimulate β cell autophagy, e.g., via FoxO1, thereby protecting against β cell stress [ 162 , 163 ].…”

Section: Type 2 Diabetesmentioning

confidence: 99%

β Cell and Autophagy: What Do We Know?

et al. 2023

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Pancreatic β cells are central to glycemic regulation through insulin production. Studies show autophagy as an essential process in β cell function and fate. Autophagy is a catabolic cellular process that regulates cell homeostasis by recycling surplus or damaged cell components. Impaired autophagy results in β cell loss of function and apoptosis and, as a result, diabetes initiation and progress. It has been shown that in response to endoplasmic reticulum stress, inflammation, and high metabolic demands, autophagy affects β cell function, insulin synthesis, and secretion. This review highlights recent evidence regarding how autophagy can affect β cells’ fate in the pathogenesis of diabetes. Furthermore, we discuss the role of important intrinsic and extrinsic autophagy modulators, which can lead to β cell failure.

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“…Mitophagy, one specific form of autophagy, eliminates damaged or aged mitochondria to decrease reactive oxygen species (ROS) production and provides additional metabolic avenues for re-establishment of intracellular homeostasis. , Therefore, mitophagy severely lessens pyroptosis inducer-mediated antitumor performance since the pyroptosis is originated from unbalanced mitochondria with caspase activation. For instance, Li et al utilized 3-methyladenine to inhibit the autophagy process in murine tumor cells, which could significantly increase the high glucose-induced immune activation for tumor therapy . Lonidamine (LND), an effective aerobic respiration inhibitor, could disrupt mitochondrial respiration, stimulate ROS generation, and induce oxidative injury within tumor cells .…”

Section: Introductionmentioning

confidence: 99%

“…For instance, Li et al activation for tumor therapy. 17 Lonidamine (LND), an effective aerobic respiration inhibitor, could disrupt mitochondrial respiration, stimulate ROS generation, and induce oxidative injury within tumor cells. 18 In addition, LND had been reported to induce pyroptotic cell death accompanied by release of immune-activated mediators including inflammatory factors of lactic dehydrogenase (LDH), interleukin-1 β (IL-1β), and nonhistone nuclear protein of the high mobility group box-1 (HMGB1) protein.…”

Section: ■ Introductionmentioning

confidence: 99%

Mitochondria-Targeting Pyroptosis Amplifier of Lonidamine-Modified Black Phosphorus Nanosheets for Glioblastoma Treatments

Ren

Dong

et al. 2023

ACS Appl. Mater. Interfaces

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Pyroptosis is accompanied by immunogenic mediators’ release and serves as an innovative strategy to reprogram tumor microenvironments. However, damaged mitochondria, the origin of pyroptosis, are frequently eliminated by mitophagy, which will severely impair pyroptosis-elicited immune activation. Herein, black phosphorus nanosheets (BP) are employed as a pyroptosis inducer delivery and mitophagy flux blocking system since the degradation of BP could impair lysosomal function by altering the pH within lysosomes. The pyroptosis inducer of lonidamine (LND) was precoupled with the mitochondrial target moiety of triphenylphosphonium to facilitate the occurrence of pyroptosis. The mitochondria-targeting LND-modified BP (BPTLD) were further encapsulated into the macrophage membrane to endow the BPTLD with blood-brain barrier penetration and tumor-targeting capability. The antitumor activities of membrane-encapsulated BPTLD (M@BPTLD) were investigated using a murine orthotopic glioblastoma model. The results demonstrated that the engineered nanosystem of M@BPTLD could target the mitochondria, and induce as well as reinforce pyroptosis via mitophagy flux blocking, thereby boosting the release of immune-activated factors to promote the maturation of dendritic cells. Furthermore, upon near-infrared (NIR) irradiation, M@BPTLD induced stronger mitochondrial oxidative stress, which further advanced robust immunogenic pyroptosis in glioblastoma cells. Thus, this study utilized the autophagy flux inhibition and phototherapy performance of BP to amplify LND-mediated pyroptosis, which might greatly contribute to the development of pyroptosis nanomodulators.

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LncRNA MEG3 regulates autophagy and pyroptosis via FOXO1 in pancreatic β-cells

Cited by 11 publications

References 38 publications

The role of ncRNAs‐mediated pyroptosis in diabetes and its vascular complications

The role of ncRNAs‐mediated pyroptosis in diabetes and its vascular complications

β Cell and Autophagy: What Do We Know?

Mitochondria-Targeting Pyroptosis Amplifier of Lonidamine-Modified Black Phosphorus Nanosheets for Glioblastoma Treatments

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