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Cited by 185

The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.

Autophagy and Ferroptosis—What Is the Connection?

Open access
Kang, Rui, Tang, Daolin·2017·Current Pathobiology Reports

Abstract

Purpose of ReviewAutophagy is a conserved intracellular degradation system and plays a dual role in cell death, depending on context and phase. Ferroptosis is a new form of regulated cell death that mainly depends on iron accumulation and lipid peroxidation. In this review, we summarize the processes of autophagy and ferroptosis and discuss their crosstalk mechanisms at the molecular level.Recent FindingsThe original study shows that ferroptosis is morphologically, biochemically, and genetically distinct from autophagy and other types of cell death. However, recent studies demonstrate that activation of ferroptosis is indeed dependent on the induction of autophagy. Additionally, many ferroptosis regulators such as SLC7A11, GPX4, NRF2, p53, HSPB1, CISD1, FANCD2, and ACSL4 have been identified as potential regulators of autophagy.SummaryThis review not only highlights the importance of autophagy as an emerging mechanism of ferroptosis but also raises new insights regarding regulated cell death.

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Metadata

Authors
Kang, R., & Tang, D.
Venue
Current Pathobiology Reports
Published
2017-04-20
Volume
5
Issue
2
Pages
153-159
ISSN
2167-485X (ISSN-L)
OpenAlex
W2607376936
Cited by
185
References
30
FWCI
9.92
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Autophagy and Ferroptosis—What Is the Connection? https://app.cochat.ai/papers/10.1007/s40139-017-0139-5
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Kang, R., & Tang, D. (2017). Autophagy and Ferroptosis—What Is the Connection? Current Pathobiology Reports. https://doi.org/10.1007/s40139-017-0139-5

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.