ReviewBiochimica et biophysica acta2011
Cell metabolism: an essential link between cell growth and apoptosis.
Review in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
97 citing papers in PubMed, 1 synthesis or guideline pooled it, 181 citations in OpenAlex.
- The impact of cryopreservation on bone marrow-derived mesenchymal stem cells: a systematic review.Journal of translational medicine · 2019Pooled it
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- Beyond Bioenergetics: Emerging Roles of Mitochondrial Fatty Acid Oxidation in Stress Response and Aging.Cells · 2025Review
- What's on the menu?: metabolic constraints in the pancreatic tumor microenvironment.The Journal of clinical investigation · 2025Review
- MSC-derived extracellular vesicles: Precision miRNA delivery for overcoming cancer therapy resistance.Regenerative therapy · 2025Review
- Glioma grade and mortality in relation to sequence variation in the mitochondrial genome.Cancer genetics · 2025Article
- Fucoidan alleviates high sucrose-induced metabolic disorders and enhances intestinal homeostasis through modulation of Notch signaling.Journal of advanced research · 2025Article
- Exosome-based miRNA delivery: Transforming cancer treatment with mesenchymal stem cells.Regenerative therapy · 2025Review
- Antibody/siRNA Nanocarriers Against Wnt Signaling Suppress Oncogenic and Stem-Like Behavior in Triple-Negative Breast Cancer Cells.Journal of biomedical materials research. Part A · 2025Article
- Extracellular Flux Assays for the Measurement of Glycolysis and Mitochondrial Respiration in Brain Cancer Cells.Methods in molecular biology (Clifton, N.J.) · 2025Article
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- Combining human liver ECM with topographically featured electrospun scaffolds for engineering hepatic microenvironment.Scientific reports · 2024Article
- Divergent roles of ADP-ribosylation factor GTPase-activating proteins in lignocellulose utilization of Trichoderma guizhouense NJAU4742.Biotechnology for biofuels and bioproducts · 2024Article
- Chemopreventive Potential ofPharmaceuticals (Basel, Switzerland) · 2024Article
- Glycolytic enzymes in non-glycolytic web: functional analysis of the key players.Cell biochemistry and biophysics · 2024Review
- A chromosome-level genome assembly of the soybean pod borer: insights into larval transcriptional response to transgenic soybean expressing the pesticidal Cry1Ac protein.BMC genomics · 2024Article
- A Novel Fibrin Matrix Derived from Platelet-Rich Plasma: Protocol and Characterization.International journal of molecular sciences · 2024Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Growth factor-stimulated or cancerous cells require sufficient nutrients to meet the metabolic demands of cell growth and division. If nutrients are insufficient, metabolic checkpoints are triggered that lead to cell cycle arrest and the activation of the intrinsic apoptotic cascade through a process dependent on the Bcl-2 family of proteins. Given the connections between metabolism and apoptosis, the notion of targeting metabolism to induce cell death in cancer cells has recently garnered much attention. However, the signaling pathways by which metabolic stresses induce apoptosis have not as of yet been fully elucidated. Thus, the best approach to this promising therapeutic avenue remains unclear. This review will discuss the intricate links between metabolism, growth, and intrinsic apoptosis and will consider ways in which manipulation of metabolism might be exploited to promote apoptotic cell death in cancer cells. This article is part of a Special Issue entitled Mitochondria: the deadly organelle.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.