Autophagy: Regulator of cell death

Cell Death and Disease, Год журнала: 2023, Номер 14(10)

Опубликована: Окт. 4, 2023

Abstract Autophagy is the process by which cells degrade and recycle proteins organelles to maintain intracellular homeostasis. Generally, autophagy plays a protective role in cells, but disruption of mechanisms or excessive autophagic flux usually leads cell death. Despite recent progress study regulation underlying molecular autophagy, numerous questions remain be answered. How does regulate death? What are fine-tuned regulatory autophagy-dependent death (ADCD) autophagy-mediated (AMCD)? In this article, we highlight different roles discuss six main autophagy-related modalities, with focus on metabolic changes caused endoplasmic reticulum-phagy (ER-phagy)-induced mitophagy ferroptosis. Finally, enhancement treatment diseases offer new perspective based use for functional conversions (including conversion that modalities) clinical tumors.

Язык: Английский

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Immunological impact of cell death signaling driven by radiation on the tumor microenvironment

Nature Immunology, Год журнала: 2019, Номер 21(2), С. 120 - 134

Опубликована: Дек. 23, 2019

Язык: Английский

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Oxidative stress and regulated cell death in Parkinson’s disease

Ageing Research Reviews, Год журнала: 2021, Номер 67, С. 101263 - 101263

Опубликована: Фев. 2, 2021

Язык: Английский

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Reactive Oxygen Species (ROS) Regulates Different Types of Cell Death by Acting as a Rheostat

Oxidative Medicine and Cellular Longevity, Год журнала: 2021, Номер 2021(1)

Опубликована: Янв. 1, 2021

Reactive oxygen species (ROS) are essential for cellular signaling and response to stress. The level of ROS the type determine ability cells undergo cell death. Furthermore, dysregulation antioxidant pathways is associated with many diseases. It has become apparent that death can occur through different mechanisms leading classifications types such as apoptosis, ferroptosis, necroptosis. play roles in all forms death, but it only now coming into focus control occurs any given cell. Indeed, may act a rheostat allowing be engaged crosstalk types. In this review, we will describe regulatory how they under normal disease states. We also propose could provide mechanism between determining

Язык: Английский

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Quantitative proteomic analyses reveal that GPX4 downregulation during myocardial infarction contributes to ferroptosis in cardiomyocytes

Cell Death and Disease, Год журнала: 2019, Номер 10(11)

Опубликована: Ноя. 4, 2019

Abstract Ischaemic heart disease (IHD) is the leading cause of death worldwide. Although myocardial cell plays a significant role in infarction (MI), its underlying mechanism remains to be elucidated. To understand progression MI and identify potential therapeutic targets, we performed tandem mass tag (TMT)-based quantitative proteomic analysis using an mouse model. Gene ontology (GO) gene set enrichment (GSEA) revealed that glutathione metabolic pathway reactive oxygen species (ROS) were significantly downregulated during MI. In particular, peroxidase 4 (GPX4), which protects cells from ferroptosis (an iron-dependent programme regulated necrosis), was early middle stages RNA-seq qRT-PCR analyses suggested GPX4 downregulation occurred at transcriptional level. Depletion or inhibition specific siRNA chemical inhibitor RSL3, respectively, resulted accumulation lipid peroxide, by H9c2 cardiomyoblasts. neonatal rat ventricular myocytes (NRVMs) less sensitive than cells, NRVMs rapidly underwent response under cysteine deprivation. Our study suggests contributes ferroptotic cardiomyocytes upon stress such as

Язык: Английский

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