CoChat
Sign Up
Cited by 983

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

MITOCHONDRIAL DNA MUTATIONS AS AN IMPORTANT CONTRIBUTOR TO AGEING AND DEGENERATIVE DISEASES

Linnane, AnthonyW., Ozawa, Takayuki, Marzuki, Sangkot, Tanaka, Masashi·1989·The Lancet
DOI 10.1016/s0140-6736(89)92145-4
Open this paper in CoChat — free account

Abstract

The human mitochondrial genome is very small and economically packed; the expression of the whole genome is essential for the maintenance of mitochondrial bioenergetic function. Mutation occurs at a much higher rate in the mitochondrial DNA (mtDNA) than in chromosomal DNA. Transient heteroplasmy of mtDNA occurs after a mutational event; the random pattern of cytoplasmic segregation that occurs during subsequent growth gives rise to a mosaic of cells. The variable proportion of mutant mitochondrial genomes per cell results in cells with a range of bioenergetic capacities. It is proposed that the accumulation of mitochondrial mutations and the subsequent cytoplasmic segregation of these mutations during life is an important contributor both to the ageing process and to several human degenerative diseases. Replacement therapy and pharmacological support may be possible for the amelioration of such disorders by means of appropriate redox compounds. Moreover, new compounds with desired redox potentials can be rationally designed for clinical use.

Overview

Integrity signals

Registry

Crossref · 10.1016/s0140-6736(89)92145-4

Cites

1 of 1 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Show all 1 references

Research works printed but not linked: 24

  1. Attardi, 1981, Organization and expression of the mammalian mitochondrial genome. a lesson in economy, Trends Biochem Sci, 6, 86, 10.1016/0968-0004(81)90031-1 · DOI
  2. Anderson, 1981, Sequence and organization of the human mitochondrial genome, Nature, 290, 457, 10.1038/290457a0 · DOI
  3. Tzagoloff, 1986, Genetics of mitochondrial biogenesis, Annu Rev Biochem, 55, 249, 10.1146/annurev.bi.55.070186.001341 · DOI
  4. Giles, 1980, Maternal inheritance of human mitochondrial DNA, Proc Nail Acad Sci USA, 77, 6715, 10.1073/pnas.77.11.6715 · DOI · Paper page
  5. Brown, 1979, Rapid evolution of animal mitochondrial DNA, Proc Natl Acad Sci USA, 76, 1967, 10.1073/pnas.76.4.1967 · DOI · Paper page
  6. Linnane, 1972, The biogenesis of mitochondria in microorganisms, Annu Rev Microbiol, 26, 163, 10.1146/annurev.mi.26.100172.001115 · DOI
  7. Linnane, 1978, Mitochondrial genetics in perspective. the derivative of a genetic and physical map of the yeast mitochondrial genome, Plasmid, 1, 324, 10.1016/0147-619X(78)90049-5 · DOI
  8. Burn, 1977, Mitotic segregation of cytoplasmic determinants for chloramphenicol resistance in mammalian cells I fusion with mouse cell lines, Somatic Cell Genet, 3, 71, 10.1007/BF01550988 · DOI
  9. Bunn, 1977, Carbomycin resistance in mouse L cells, Somatic Cell Genet, 3, 611, 10.1007/BF01539069 · DOI
  10. Wallace, 1977, Mitotic segregation of cytoplasmic determinants for chloramphenicol resistance in mammalian cells II: fusions with human cell lines, Somatic Cell Genet, 3, 93, 10.1007/BF01550989 · DOI
  11. Petty, 1986, The clinical features of mitochondrial myopathy, Brain, 109, 915, 10.1093/brain/109.5.915 · DOI · Paper page
  12. DiMauro, 1987, Mitochondrial myopathies, J Inher Metab Dis, 10, 113, 10.1007/BF01812852 · DOI
  13. Byme, 1988, Current perspectives in the study of human mitochondriopathies, Med J Aust, 149, 30, 10.5694/j.1326-5377.1988.tb120480.x · DOI
  14. Holt, 1988, Deletions of muscle mitochondrial DNA in patients with mitochondrial myopathies, Nature, 331, 717, 10.1038/331717a0 · DOI
  15. Lestienne, 1988, Keams-Sayre syndrome with muscle mitochondrial DNA deletion, Lancet, i, 885, 10.1016/S0140-6736(88)91632-7 · DOI
  16. Holt, 1988, Deletions of muscle mitochondrial DNA, Lancet, 1, 1462, 10.1016/S0140-6736(88)92273-8 · DOI
  17. Rotig, 1988, Deletion of blood mitochondrial DNA in pancytopenia, Lancet, ii, 567, 10.1016/S0140-6736(88)92687-6 · DOI
  18. Piko, 1988, Studies of sequence heterogeneity of mitochondrial DNA from rat and mouse tissues evidence for an increased frequency of deletions/additions with aging, Mech Ageing Dev, 43, 279, 10.1016/0047-6374(88)90037-1 · DOI
  19. Ozawa, 1987, Maternal inheritance of deleted mitochondrial DNA in a family with mitochondrial myopathy, Biochem Biophys Res Commun, 154, 1240, 10.1016/0006-291X(88)90272-0 · DOI
  20. Noer, 1988, Mitochondrial DNA deletion in encephalomyopathy, Lancet, ii, 1253, 10.1016/S0140-6736(88)90847-1 · DOI
  21. Robin, 1988, Mitochondrial DNA molecules and virtual number of mitochondria per cell in mammalian cells, J Cell Physiol, 136, 507, 10.1002/jcp.1041360316 · DOI
  22. Ozawa, 1987, Structure and function of mitochondria. their organization and disorders, Brain Dev, 9, 76, 10.1016/S0387-7604(87)80021-9 · DOI
  23. Ichiki, 1988, Deficiency of subunits of complex I and mitochondrial encephalomyopathy, Ann Neurol, 23, 287, 10.1002/ana.410230312 · DOI
  24. Eleff, 1984, NMR study of improvement in oxidative phosphorylation by vitamins K3 and C in a patient with a defect in electron transport at complex III in skeletal muscle, Proc Natl Acad Sci USA, 81, 529, 10.1073/pnas.81.11.3529 · DOI

Cited by

Sorted by citations

Metadata

Authors
Linnane, A., Ozawa, T., Marzuki, S., & Tanaka, M.
Venue
The Lancet
Publisher
Elsevier BV
Published
1989-03
Volume
333
Issue
8639
Pages
642-645
ISSN
0140-6736
DOI
10.1016/s0140-6736(89)92145-4
Cited by
983
References
1
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review