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Cited by 1,306Genetics, Aging, and Longevity in Model OrganismsEvolution and Genetic DynamicsRenal Diseases and Glomerulopathies

Evolutionary biology of aging

Michael R. Rose·1991·Choice Reviews Online
DOI 10.5860/choice.28-5664
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Abstract

Reviews 469 giving a picture of hereditary renal disorders at a number of (mainly Italian) nephrological centers.About 18 mo elapsed between the meeting and publication.Events have moved on apace.It was then known that, in addition to the two major components of collagen IV, a third chain also existed.Five separately coded constituents of collagen IV are now recognized.The fifth chain is known to be encoded on the X chromosome, in the same map area as Alport syndrome.This gene has been cloned by two independent groups (Hostikka et al. 1990; Myers et al. 1990).About 10% of Alport syndrome patients show gross gene rearrangements, establishing that classical Alport syndrome is a disorder of this one component of basement membrane collagen.This is very substantial progress, but the pathogenesis of the renal disorder, the relationship of the gene abnormality to the extrarenal signs of the disorder, the possibility of locus heterogeneity within Alport syndrome, and the molecular genetics of the other inherited nephritides all remain to be elucidated.Despite having just missed the major advance in understanding Alport syndrome, this book poses many clinical and pathological questions that remain valid sign- posts for the way ahead.

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  • Evolutionary theory says aging results from weakening natural selection with age.

    “Evolutionary theory holds that aging is a consequence of the declining force of natural selection with age (1).”

    From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [1]

  • Few old survivors remain for selection to remove late-acting harmful alleles.

    “Consequently, there are generally few old survivors on which natural selection can act to eliminate alleles or genes that have late-acting deleterious effects.”

    From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [1]

  • External hazards limit lifespan and reduce older individuals in natural populations.

    “Extrinsic hazards—accidents, predation, infection, starvation, and so forth—limit the life span of most species, thereby depleting natural populations of older individuals.”

    From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [1]

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Authors
Rose, M. R.
Corresponding author
Michael R. Rose
ORCID
Michael R. Rose
Venue
Choice Reviews Online
Publisher
American Library Association
Published
1991-06-01
Volume
28
Issue
10
Pages
28-5664-28-5664
ISSN
  • 0009-4978 (ISSN-L)
  • 1523-8253
DOI
10.5860/choice.28-5664
OpenAlex
W1540286737
Cited by
1,306
References
0
Citations by year
2025: 10 · 2024: 17 · 2023: 9 · 2022: 6 · 2021: 27 · 2020: 19 · 2019: 25 · 2018: 57 · 2017: 30 · 2016: 28 · 2015: 31 · 2014: 31 · 2013: 38 · 2012: 37
Type
book review
Language
en
Open access
closed
Locations
Choice Reviews Online (publishedVersion)
Funders
March of Dimes Foundation
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Evolution and Genetic Dynamics
  • Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
Keywords
aging, evolutionary biology of aging, Alport syndrome, type IV collagen, basement membrane, locus heterogeneity, molecular genetics

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