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Open accessJournalISSN: 2041-4889

Cell Death and Disease

About: Cell Death and Disease is an academic journal. The journal publishes majorly in the area(s): Programmed cell death & Apoptosis. It has an ISSN identifier of 2041-4889. It is also open access. Over the lifetime, 7303 publication(s) have been published receiving 206947 citation(s).

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Topics: Programmed cell death, Apoptosis, Autophagy ...read more
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Open accessJournal ArticleDOI: 10.1038/CDDIS.2013.350
Xinbing Sui1, R Chen1, Z Wang1, Z Huang1  +9 moreInstitutions (1)
Abstract: Induction of cell death and inhibition of cell survival are the main principles of cancer therapy. Resistance to chemotherapeutic agents is a major problem in oncology, which limits the effectiveness of anticancer drugs. A variety of factors contribute to drug resistance, including host factors, specific genetic or epigenetic alterations in the cancer cells and so on. Although various mechanisms by which cancer cells become resistant to anticancer drugs in the microenvironment have been well elucidated, how to circumvent this resistance to improve anticancer efficacy remains to be defined. Autophagy, an important homeostatic cellular recycling mechanism, is now emerging as a crucial player in response to metabolic and therapeutic stresses, which attempts to maintain/restore metabolic homeostasis through the catabolic lysis of excessive or unnecessary proteins and injured or aged organelles. Recently, several studies have shown that autophagy constitutes a potential target for cancer therapy and the induction of autophagy in response to therapeutics can be viewed as having a prodeath or a prosurvival role, which contributes to the anticancer efficacy of these drugs as well as drug resistance. Thus, understanding the novel function of autophagy may allow us to develop a promising therapeutic strategy to enhance the effects of chemotherapy and improve clinical outcomes in the treatment of cancer patients.

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Topics: Autophagy (53%), Programmed cell death (52%), Cancer (51%)

806 Citations


Open accessJournal ArticleDOI: 10.1038/CDDIS.2013.60
Yuhua Zhao1, Ethan B. Butler2, Ming Tan2Institutions (2)
Abstract: The metabolic properties of cancer cells diverge significantly from those of normal cells. Energy production in cancer cells is abnormally dependent on aerobic glycolysis. In addition to the dependency on glycolysis, cancer cells have other atypical metabolic characteristics such as increased fatty acid synthesis and increased rates of glutamine metabolism. Emerging evidence shows that many features characteristic to cancer cells, such as dysregulated Warburg-like glucose metabolism, fatty acid synthesis and glutaminolysis are linked to therapeutic resistance in cancer treatment. Therefore, targeting cellular metabolism may improve the response to cancer therapeutics and the combination of chemotherapeutic drugs with cellular metabolism inhibitors may represent a promising strategy to overcome drug resistance in cancer therapy. Recently, several review articles have summarized the anticancer targets in the metabolic pathways and metabolic inhibitor-induced cell death pathways, however, the dysregulated metabolism in therapeutic resistance, which is a highly clinical relevant area in cancer metabolism research, has not been specifically addressed. From this unique angle, this review article will discuss the relationship between dysregulated cellular metabolism and cancer drug resistance and how targeting of metabolic enzymes, such as glucose transporters, hexokinase, pyruvate kinase M2, lactate dehydrogenase A, pyruvate dehydrogenase kinase, fatty acid synthase and glutaminase can enhance the efficacy of common therapeutic agents or overcome resistance to chemotherapy or radiotherapy.

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Topics: Glutaminolysis (56%), Lactate dehydrogenase A (56%), Pyruvate dehydrogenase kinase (55%) ...read more

771 Citations


Open accessJournal ArticleDOI: 10.1038/CDDIS.2016.105
Abstract: Tumor cells harbor genetic alterations that promote a continuous and elevated production of reactive oxygen species. Whereas such oxidative stress conditions would be harmful to normal cells, they facilitate tumor growth in multiple ways by causing DNA damage and genomic instability, and ultimately, by reprogramming cancer cell metabolism. This review outlines the metabolic-dependent mechanisms that tumors engage in when faced with oxidative stress conditions that are critical for cancer progression by producing redox cofactors. In particular, we describe how the mitochondria has a key role in regulating the interplay between redox homeostasis and metabolism within tumor cells. Last, we will discuss the potential therapeutic use of agents that directly or indirectly block metabolism.

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Topics: Oxidative stress (55%), Cancer cell (53%), DNA damage (51%)

615 Citations


Open accessJournal ArticleDOI: 10.1038/CDDIS.2015.327
Fei Gao1, Sm M. Chiu1, Dal A. L. Motan1, Zhao Zhang1  +5 moreInstitutions (3)
Abstract: The unique immunomodulatory properties of mesenchymal stem cells (MSCs) make them an invaluable cell type for the repair of tissue/ organ damage caused by chronic inflammation or autoimmune disorders. Although they hold great promise in the treatment of immune disorders such as graft versus host disease (GvHD) and allergic disorders, there remain many challenges to overcome before their widespread clinical application. An understanding of the biological properties of MSCs will clarify the mechanisms of MSC-based transplantation for immunomodulation. In this review, we summarize the preclinical and clinical studies of MSCs from different adult tissues, discuss the current hurdles to their use and propose the future development of pluripotent stem cell-derived MSCs as an approach to immunomodulation therapy.

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600 Citations


Open accessJournal ArticleDOI: 10.1038/CDDIS.2009.16
Ellen Wirawan1, L Vande Walle1, Kristof Kersse1, Sigrid Cornelis1  +11 moreInstitutions (3)
Abstract: Autophagy and apoptosis are two important and interconnected stress-response mechanisms. However, the molecular interplay between these two pathways is not fully understood. To study the fate and function of autophagic proteins at the onset of apoptosis, we used a cellular model system in which autophagy precedes apoptosis. IL-3 depletion of Ba/F3 cells caused caspase (casp)-mediated cleavage of Beclin-1 and PI3KC3, two crucial components of the autophagy-inducing complex. We identified two casp cleavage sites in Beclin-1, TDVD133 and DQLD149, cleavage at which yields fragments lacking the autophagy-inducing capacity. Noteworthy, the C-terminal fragment, Beclin-1-C, localized predominantly at the mitochondria and sensitized the cells to apoptosis. Moreover, on isolated mitochondria, recombinant Beclin-1-C was able to induce the release of proapoptotic factors. These findings point to a mechanism by which casp-dependent generation of Beclin-1-C creates an amplifying loop enhancing apoptosis upon growth factor withdrawal.

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Topics: Programmed cell death (61%), Autophagy (59%), Caspase (52%) ...read more

538 Citations


Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
20211,081
20201,023
2019931
20181,226
2017646
2016464

Top Attributes

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Journal's top 5 most impactful authors

Guido Kroemer

38 papers, 1.1K citations

Gerry Melino

22 papers, 920 citations

Andreas Strasser

16 papers, 482 citations

Toshihide Yamashita

11 papers, 202 citations

Peter Vandenabeele

10 papers, 1.1K citations

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