ReviewCell calcium2008
Mitochondrial Ca2+ homeostasis in lysosomal storage diseases.
Review in Cell calcium, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 35 citations in OpenAlex.
- Lipofuscin accumulation in aging and neurodegeneration: a potential "timebomb" overlooked in Alzheimer's disease.Translational neurodegeneration · 2025Review
- Inflammation, Oxidative Stress, and Endothelial Dysfunction in the Pathogenesis of Vascular Damage: Unraveling Novel Cardiovascular Risk Factors in Fabry Disease.International journal of molecular sciences · 2024Review
- Lysosomes in retinal health and disease.Trends in neurosciences · 2023Review
- NDST3 deacetylates α-tubulin and suppresses V-ATPase assembly and lysosomal acidification.The EMBO journal · 2021Article
- Pathogenesis and Molecular Mechanisms of Anderson-Fabry Disease and Possible New Molecular Addressed Therapeutic Strategies.International journal of molecular sciences · 2021Review
- Rapid Identification of New Biomarkers for the Classification of GM1 Type 2 Gangliosidosis Using an UnbiasedCells · 2021Article
- Interplay Between Lipid Metabolism and Autophagy.Frontiers in cell and developmental biology · 2020Review
- Mitochondrial adventures at the organelle society.Biochemical and biophysical research communications · 2018Review
- Linking mitochondrial dysfunction to neurodegeneration in lysosomal storage diseases.Journal of inherited metabolic disease · 2017Review
- Altered Cellular Homeostasis in Murine MPS I Fibroblasts: Evidence of Cell-Specific Physiopathology.JIMD reports · 2017Article
- Lysosomal and Mitochondrial Liaisons in Niemann-Pick Disease.Frontiers in physiology · 2017Review
- Integrated analysis of proteome and transcriptome changes in the mucopolysaccharidosis type VII mouse hippocampus.Molecular genetics and metabolism · 2016Article
- The Mitochondrial Permeability Transition Pore: Channel Formation by F-ATP Synthase, Integration in Signal Transduction, and Role in Pathophysiology.Physiological reviews · 2015Review
- Role of extracellular calcium and mitochondrial oxygen species in psychosine-induced oligodendrocyte cell death.Cell death & disease · 2014Article
- Effects of chronic exposure to cigarette smoke on canonical transient receptor potential expression in rat pulmonary arterial smooth muscle.American journal of physiology. Cell physiology · 2014Article
- Combination therapies for lysosomal storage disease: is the whole greater than the sum of its parts?Human molecular genetics · 2011Review
- Three-dimensional structure of Rubella virus factories.Virology · 2010Article
- Pathophysiology of neuropathic lysosomal storage disorders.Journal of inherited metabolic disease · 2010Review
- Aberrant Ca2+ handling in lysosomal storage disorders.Cell calcium · 2010Review
- A double TRPtych: six views of transient receptor potential channels in disease and health.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Review
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 2 institutions in 1 country.
Funding
Abstract
Lysosomal storage diseases (LSDs) are a class of genetic disorders in which proteins responsible for digestion or absorption of endocytosed material do not function or do not localize properly. The resulting cellular "indigestion" causes buildup of intracellular storage inclusions that contain unprocessed lipids and proteins that form macromolecular complexes. The buildup of storage material is associated with degenerative processes that are observed in all LSDs, albeit the correlation between the amount of storage inclusions and the severity of the degenerative processes is not always evident. The latter suggests that a specific mechanism set in motion by aberrant lysosomal function drives the degenerative processes in LSDs. It is becoming increasingly clear that in addition to their function in degrading endocytosed material, lysosomes are essential housekeeping organelles responsible for maintaining healthy population of intracellular organelles, in particular mitochondria. The present review surveys the current knowledge on the lysosomal-mitochondrial axis and its possible role as a contributing factor to mitochondrial Ca(2+) homeostasis and to cell death in LSDs.
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.