ReviewTrends in endocrinology and metabolism: TEM2009
Mitochondrial protein phosphorylation: instigator or target of lipotoxicity?
Review in Trends in endocrinology and metabolism: TEM, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 25 citations in OpenAlex.
- The effect of dietary habits on oocyte/sperm quality.Journal of the Turkish German Gynecological Association · 2023Article
- The anti-aging effects of Renshen Guben on thyrotoxicosis mice: Improving immunosenescence, hypoproteinemia, lipotoxicity, and intestinal flora.Frontiers in immunology · 2022Article
- Low-Level Saturated Fatty Acid Palmitate Benefits Liver Cells by Boosting Mitochondrial Metabolism via CDK1-SIRT3-CPT2 Cascade.Developmental cell · 2020Article
- Dysregulation of Sqstm1, mitophagy, and apoptotic genes in chronic exposure to arsenic and high-fat diet (HFD).Environmental science and pollution research international · 2018Article
- PPARs and Metabolic Disorders Associated with Challenged Adipose Tissue Plasticity.International journal of molecular sciences · 2018Review
- Mitochondria and ageing: role in heart, skeletal muscle and adipose tissue.Journal of cachexia, sarcopenia and muscle · 2017Review
- Metabolic control of oocyte development: linking maternal nutrition and reproductive outcomes.Cellular and molecular life sciences : CMLS · 2015Review
- Apolipoprotein O is mitochondrial and promotes lipotoxicity in heart.The Journal of clinical investigation · 2014Article
- Mitochondria in the pathogenesis of diabetes: a proteomic view.Protein & cell · 2012Review
- Endothelial mitochondria--less respiration, more integration.Pflugers Archiv : European journal of physiology · 2012Review
- Long-term treatment with the pan-PPAR agonist tetradecylthioacetic acid or fish oil is associated with increased cardiac content of n-3 fatty acids in rat.Lipids in health and disease · 2012Article
- A murine model of isolated cardiac steatosis leads to cardiomyopathy.Hypertension (Dallas, Tex. : 1979) · 2011Article
- Uncoupling protein 3 adjusts mitochondrial Ca(2+) uptake to high and low Ca(2+) signals.Cell calcium · 2010Article
- Glucolipotoxicity of the pancreatic beta cell.Biochimica et biophysica acta · 2010Review
- Expression profiling of mouse embryonic fibroblasts with a deletion in the helicase domain of the Werner Syndrome gene homologue treated with hydrogen peroxide.BMC genomics · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Lipotoxicity occurs as a consequence of chronic exposure of non-adipose tissue and cells to elevated concentrations of fatty acids, triglycerides and/or cholesterol. The contribution of mitochondria to lipotoxic cell dysfunction, damage and death is associated with elevated production of reactive oxygen species and initiation of apoptosis. Although there is a broad consensus on the involvement of these phenomena with lipotoxicity, the molecular mechanisms that initiate, mediate and trigger mitochondrial dysfunction in response to substrate overload remain unclear. Here, we focus on protein phosphorylation as an important phenomenon in lipotoxicity that harms mitochondria-related signal transduction and integration in cellular metabolism. Moreover, the degradation of mitochondria by mitophagy is discussed as an important landmark that leads to cellular apoptosis in lipotoxicity.
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.