51
© Springer Nature Switzerland AG 2018
S. Gerecht (ed.), Biophysical Regulation of Vascular Differentiation and
Assembly, Biological and Medical Physics, Biomedical Engineering,
https://doi.org/10.1007/978-3-319-99319-5_3
Chapter 3
Physiological and Pathological Vascular
Aging
Patrícia R. Pitrez, Helena R. Aires, Inês Tomé, Rita Sá Ferreira,
and Lino Ferreira
3.1 Introduction
It is expected that by 2030 the number of people aged 60 years and over will grow
by 56% [121]. Aging is recognized as the key factor in most chronic diseases,
including neurodegenerative, cerebrovascular, and cardiovascular disorders, through
the accumulation of biological changes over time [84]. Thus, age-related biological
changes have emerged as a serious issue, with increased socioeconomic and healthcare burdens. Several hallmarks of aging in mammals have been identified including telomere attrition, genomic instability, epigenetic modifications, loss of
proteostasis, cellular senescence, mitochondrial dysfunction, altered intercellular
communication, deregulated nutrient sensing, and stem cell exhaustion [55, 67, 93].
A major trigger for cellular aging and senescence is telomere shortening [3, 67].
Indeed, a cell’s finite replication capacity is promoted by telomere shortening [52].
Telomeres are repeats of highly conserved nucleotide sequences that compose the
chromosome ends to prevent chromosome fusion [52]. Mammalian cells do not
express telomerase, the enzyme responsible for telomere replication, and because
the enzyme is consumed at each cell cycle, telomeres become shorter until they cannot prevent a DNA damage response [20, 127]. Another trigger for normal aging is
P. R. Pitrez · H. R. Aires · I. Tomé
Faculty of Medicine, University of Coimbra, Coimbra, Portugal
e-mail: pitrezpatricia@uc.pt
R. S. Ferreira
Center of Neurosciences and Cell Biology, University of Coimbra, Coimbra, Portugal
L. Ferreira (*)
Faculty of Medicine, University of Coimbra, Coimbra, Portugal
Center of Neurosciences and Cell Biology, University of Coimbra, Coimbra, Portugal
e-mail: lino@uc-biotech.pt
© Springer Nature Switzerland AG 2018
S. Gerecht (ed.), Biophysical Regulation of Vascular Differentiation and
Assembly, Biological and Medical Physics, Biomedical Engineering,
https://doi.org/10.1007/978-3-319-99319-5_3
Chapter 3
Physiological and Pathological Vascular
Aging
Patrícia R. Pitrez, Helena R. Aires, Inês Tomé, Rita Sá Ferreira,
and Lino Ferreira
3.1 Introduction
It is expected that by 2030 the number of people aged 60 years and over will grow
by 56% [121]. Aging is recognized as the key factor in most chronic diseases,
including neurodegenerative, cerebrovascular, and cardiovascular disorders, through
the accumulation of biological changes over time [84]. Thus, age-related biological
changes have emerged as a serious issue, with increased socioeconomic and healthcare burdens. Several hallmarks of aging in mammals have been identified including telomere attrition, genomic instability, epigenetic modifications, loss of
proteostasis, cellular senescence, mitochondrial dysfunction, altered intercellular
communication, deregulated nutrient sensing, and stem cell exhaustion [55, 67, 93].
A major trigger for cellular aging and senescence is telomere shortening [3, 67].
Indeed, a cell’s finite replication capacity is promoted by telomere shortening [52].
Telomeres are repeats of highly conserved nucleotide sequences that compose the
chromosome ends to prevent chromosome fusion [52]. Mammalian cells do not
express telomerase, the enzyme responsible for telomere replication, and because
the enzyme is consumed at each cell cycle, telomeres become shorter until they cannot prevent a DNA damage response [20, 127]. Another trigger for normal aging is
P. R. Pitrez · H. R. Aires · I. Tomé
Faculty of Medicine, University of Coimbra, Coimbra, Portugal
e-mail: pitrezpatricia@uc.pt
R. S. Ferreira
Center of Neurosciences and Cell Biology, University of Coimbra, Coimbra, Portugal
L. Ferreira (*)
Faculty of Medicine, University of Coimbra, Coimbra, Portugal
Center of Neurosciences and Cell Biology, University of Coimbra, Coimbra, Portugal
e-mail: lino@uc-biotech.pt