ReviewAnnals of the New York Academy of Sciences2010
Bioenergetics and cell death.
Review in Annals of the New York Academy of Sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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
54 citing papers in PubMed.
- Article
- Disruption of Calcium Homeostasis in Human Spermatozoa: Implications on Mitochondrial Bioenergetics, ROS Production, Phosphatidylserine Externalization, and Motility.Antioxidants (Basel, Switzerland) · 2026Article
- Asexual reproduction in reef-building corals: insights into fragment attachment to improve restoration and predict natural recovery.Royal Society open science · 2025Article
- Morin as a Modulator of Hepatic Glucose Fluxes: A Balance Between Antihyperglycemic Potential and Mitochondrial Toxicity.Journal of biochemical and molecular toxicology · 2025Article
- Article
- Fibrillar tau alters cerebral endothelial cell metabolism, vascular inflammatory activation, and barrier function in vitro and in vivo.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- MCU-i4, a mitochondrial CaOncology research · 2025Article
- Dose-dependent effects of acetaminophen and ibuprofen on mitochondrial respiration of human platelets.Molecular and cellular biochemistry · 2024Article
- Preclinical assessment of MAGMAS inhibitor as a potential therapy for pediatric medulloblastoma.PloS one · 2024Article
- Ultrastructural features mirror metabolic derangement in human endothelial cells exposed to high glucose.Scientific reports · 2023Article
- COPA3 peptide supplementation alleviates the heat stress of chicken fibroblasts.Frontiers in veterinary science · 2023Article
- Anastasis: cell recovery mechanisms and potential role in cancer.Cell communication and signaling : CCS · 2022Review
- Modeling apoptosis resistance in CHO cells with CRISPR-mediated knockouts of Bak1, Bax, and Bok.Biotechnology and bioengineering · 2022Article
- Disruption of mitochondrial quality control genes promotes caspase-resistant cell survival following apoptotic stimuli.The Journal of biological chemistry · 2022Article
- The Role of Mitochondrial miRNAs in the Development of Radon-Induced Lung Cancer.Biomedicines · 2022Review
- Evidence That Substantia Nigra Pars Compacta Dopaminergic Neurons Are Selectively Vulnerable to Oxidative Stress Because They Are Highly Metabolically Active.Frontiers in cellular neuroscience · 2022Review
- Combination of Ascorbic Acid and Menadione Induces Cytotoxic Autophagy in Human Glioblastoma Cells.Oxidative medicine and cellular longevity · 2022Article
- MitomiRs: their roles in mitochondria and importance in cancer cell metabolism.Radiology and oncology · 2021Review
- Cell-Permeable Succinate Rescues Mitochondrial Respiration in Cellular Models of Amiodarone Toxicity.International journal of molecular sciences · 2021Article
- Anticancer Activity of the Acetylenic Derivative of Betulin Phosphate Involves Induction of Necrotic-Like Death in Breast Cancer Cells In Vitro.Molecules (Basel, Switzerland) · 2021Article
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.
Funding
Abstract
Mitochondrial bioenergetic function is a key to cell life and death. Cells need energy not only to support their vital functions but also to die gracefully. Execution of an apoptotic program includes energy-dependent steps, including kinase signaling, formation of the apoptosome, and effector caspase activation. Under conditions of bioenergetic collapse, cells are diverted toward necrotic demise. Mitochondrial outer membrane permeabilization (MOMP) is a decisive event in the execution of apoptosis. It is also causally linked to a decline in bioenergetic function via different mechanisms, not merely due to cytochrome c dispersion. MOMP-induced bioenergetic deficiency is usually irreversible and commits cells to die, even when caspases are inactive. Here, we discuss the mechanisms by which MOMP impacts bioenergetics in different cell death paradigms.
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.