Stress and biological aging

Simm, Andreas; Klotz, Lars‐Oliver

doi:10.1007/s00391-015-0928-6

Cited by 6 publications

(6 citation statements)

References 57 publications

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“…Longevity is a multifactorial condition, affected by environmental and genetic factors, as well as by oxidative and genomic damage. Several hypotheses have been postulated to explain aging and lifespan, which have attracted widespread scientific and public interest ( Brooks-Wilson, 2013 ; Simm and Klotz, 2015 ). The reactive oxygen species (ROS) theory of aging is related to oxidative stress and macromolecule damage.…”

Section: Introductionmentioning

confidence: 99%

An association study of FOXO3 variant and longevity

et al. 2018

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Human longevity is a polygenic and multifactorial trait. Pathways related to lifespan are complex and involve molecular, cellular, and environmental processes. In this analytical observational study, we evaluated the relationship between environment factors, oxidative stress status, DNA integrity level, and the association of FOXO3 (rs2802292), SOD2 (rs4880), APOE (rs429358 and rs7412), and SIRT1 (rs2273773) polymorphisms with longevity in oldest-old individuals from southeastern Brazil. We found an association between the FOXO3 GG genotype and gender. While lifestyle, anthropometric, and biochemical characteristics showed significant results, DNA damage and oxidative stress were not related to lifespan. We found that long-lived individuals with FOXO3 GT genotype had low levels of triglycerides. This study is the first to demonstrate that FOXO3 could be a candidate gene for longevity in the Brazilian population. These results are important in terms of provisions of health care for age-related diseases and lifespan, and provide insight for further research on epigenetic, gene regulation, and expression in oldest-old individuals.

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Section: Introductionmentioning

confidence: 99%

An association study of FOXO3 variant and longevity

et al. 2018

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“…Psychological stressors, linked with the genetic and epigenetic modifications, are known as the influential causal events changing the physiology of many organs of the human body (including brain and gut [ 167 ]) and systems (including an immune [ 168 ] and hormonal [ 36 ]). Aging, accompanied by the decline in health, independence, perceptual, cognitive, and decision-making abilities, is closely associated with the negative impacts of typical psychological stress [ 6 , 169 , 170 ]. Indeed, both psychological stress and aging show cumulative impact on most physiological systems [ 171 , 172 , 173 ] involving biological events at the molecular [ 173 ], cellular [ 174 ] and system [ 34 , 41 ] levels.…”

Section: Discussionmentioning

confidence: 99%

Fundamental Clock of Biological Aging: Convergence of Molecular, Neurodegenerative, Cognitive and Psychiatric Pathways: Non-Equilibrium Thermodynamics Meet Psychology

Dyakin

Dyakina-Fagnano

McIntire

et al. 2021

IJMS

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In humans, age-associated degrading changes, widely observed in molecular and cellular processes underly the time-dependent decline in spatial navigation, time perception, cognitive and psychological abilities, and memory. Cross-talk of biological, cognitive, and psychological clocks provides an integrative contribution to healthy and advanced aging. At the molecular level, genome, proteome, and lipidome instability are widely recognized as the primary causal factors in aging. We narrow attention to the roles of protein aging linked to prevalent amino acids chirality, enzymatic and spontaneous (non-enzymatic) post-translational modifications (PTMs SP), and non-equilibrium phase transitions. The homochirality of protein synthesis, resulting in the steady-state non-equilibrium condition of protein structure, makes them prone to multiple types of enzymatic and spontaneous PTMs, including racemization and isomerization. Spontaneous racemization leads to the loss of the balanced prevalent chirality. Advanced biological aging related to irreversible PTMs SP has been associated with the nontrivial interplay between somatic (molecular aging) and mental (psychological aging) health conditions. Through stress response systems (SRS), the environmental and psychological stressors contribute to the age-associated “collapse” of protein homochirality. The role of prevalent protein chirality and entropy of protein folding in biological aging is mainly overlooked. In a more generalized context, the time-dependent shift from enzymatic to the non-enzymatic transformation of biochirality might represent an important and yet underappreciated hallmark of aging. We provide the experimental arguments in support of the racemization theory of aging.

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“…Aging is a complex biological process that involves various cellular, molecular and structural changes based on several mechanisms . Accumulating studies found that aging of functional cells was detected in the lungs of asthma patients .…”

Section: Discussionmentioning

confidence: 99%

“…Biological aging includes various cellular, molecular and structural changes based on several theories . Although usually age‐related, biological aging can also occur in early life, partially independent of age .…”

Section: Introductionmentioning

confidence: 99%

ITGB4 deficiency induces senescence of airway epithelial cells through p53 activation

Lin

Tang

et al. 2019

The FEBS Journal

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Aging is characterized by a progressive loss of physiological integrity, leading to impaired organ function and, ultimately, increased vulnerability to death. Many complex diseases are related to aging, including asthma. In the lung, the airway epithelium serves as the first barrier to prevent the access of inspired external stimuli and dictates the initial stress responses. Notably, in the airway mucosa of asthma patients, an increase in senescent airway epithelial cells has been detected. Although it has been speculated that the senescence of airway epithelial cells could increase asthma susceptibility and aggravate asthma severity, the role of cell senescence in the development of asthma remains unclear. Integrin β4 (ITGB4) is a structural adhesion molecule with complex physiological functions that is downregulated in airway epithelial cells of asthma patients. This study demonstrates that the expression of ITGB4 in airway epithelial cells is downregulated significantly under oxidative stress or upon inflammatory stimulation. Moreover, we show that ITGB4 deficiency induces the senescence of airway epithelial cells through the activation of the p53 pathway both in vitro and in vivo. Together, our results demonstrate that airway epithelial senescence induced by ITGB4 deficiency after oxidative stress or inflammatory stimulation may be involved in the pathogenesis of asthma. Understanding the contribution of ITGB4 deficiency to the senescence of airway epithelial cells in asthma patients may provide new therapeutic approaches for the treatment of asthma.

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Stress and biological aging

Cited by 6 publications

References 57 publications

An association study of FOXO3 variant and longevity

An association study of FOXO3 variant and longevity

Fundamental Clock of Biological Aging: Convergence of Molecular, Neurodegenerative, Cognitive and Psychiatric Pathways: Non-Equilibrium Thermodynamics Meet Psychology

ITGB4 deficiency induces senescence of airway epithelial cells through p53 activation

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