ReviewMolecular and cellular biochemistry2014
Mitochondrial epigenetics in bone remodeling during hyperhomocysteinemia.
Review in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
What it found
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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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Effect of B vitamin (folate, B6, and B12) supplementation on osteoporotic fracture and bone turnover markers: a meta-analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015Pooled it
- Methylmalonic Acid in Skeletal Aging and Osteoporosis: Linking Vitamin B12 Metabolism to Mitochondrial Dysfunction.Calcified tissue international · 2026Review
- Small organic molecules containing amorphous calcium phosphate: synthesis, characterization and transformation.Frontiers in bioengineering and biotechnology · 2023Article
- PGC-1α in osteoarthritic chondrocytes: From mechanism to target of action.Frontiers in pharmacology · 2023Review
- Artificial Mitochondrial Transfer (AMT) for the Management of Age-related Musculoskeletal Degenerative Disorders: An Emerging Avenue for Bone and Cartilage Metabolism Regulation.Stem cell reviews and reports · 2022Article
- Notoginsenoside R1 attenuates oxidative stress-induced osteoblast dysfunction through JNK signalling pathway.Journal of cellular and molecular medicine · 2021Article
- Mitoepigenetics and Its Emerging Roles in Cancer.Frontiers in cell and developmental biology · 2020Review
- Epigenetic regulation of bone remodeling by natural compounds.Pharmacological research · 2019Review
- Homocysteine causes dysfunction of chondrocytes and oxidative stress through repression of SIRT1/AMPK pathway: A possible link between hyperhomocysteinemia and osteoarthritis.Redox biology · 2018Article
- Toll-like receptor 4 mediates vascular remodeling in hyperhomocysteinemia.Molecular and cellular biochemistry · 2017Review
- Methionine-Restricted Diet Increases miRNAs That Can Target RUNX2 Expression and Alters Bone Structure in Young Mice.Journal of cellular biochemistry · 2017Article
- Epigenetic Regulation of Oxidative Stress in Ischemic Stroke.Aging and disease · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Increased levels of homocysteine (Hcy), known as hyperhomocysteinemia (HHcy), is an independent risk factor of various diseases. Clinical studies report that people born with severe HHcy develop skeletal malformations with weaker bone. Studies also report that altered mitochondrial dynamics and altered epigenetics contribute to weaker bones and bone diseases. Although Hcy-induced mitochondrial dysfunction has been shown to affect bone metabolism, the role of mitochondrial epigenetics (mito-epigenetics) has not been studied in bones. The epigenetics in mitochondria is interesting as the mitochondrial genome size is small (16 kb) with fewer CpG, and without histones and introns. Recently, fascinating works on epigenetics along with the discovery of histone-like proteins in mitochondria are giving exciting areas for novel studies on mitochondria epigenetics. There are mutual cause and effect relationships between bone, mitochondria, Hcy, and epigenetics, but unfortunately, studies are lacking that describe the involvement of all these together in bone disease progression. This review describes the reciprocal relationships and mechanisms of Hcy-bone-mitochondria-epigenetics along with a short discussion of techniques which could be employed to assess Hcy-induced anomaly in bone, mediated through alterations in mito-epigenetics.
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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.