Mechanisms of cellular senescence-induced vascular aging: evidence of senotherapeutic strategies DOI Open Access
Sophia Mahoney, Samuel I. Bloom,

Douglas R. Seals

et al.

The Journal of Cardiovascular Aging, Journal Year: 2025, Volume and Issue: 5(1)

Published: March 20, 2025

Cardiovascular diseases (CVD) remain the leading cause of death worldwide, with advancing age being primary, nonmodifiable risk factor. Vascular dysfunction, namely arterial stiffening and endothelial is key antecedent to development clinical CVD aging. Fundamental aging macro-mechanistic processes that drive vascular include excess oxidative stress, chronic inflammation, declines in vasodilatory molecule nitric oxide. An important hallmark contributes cellular senescence - a stress response characterized by cell cycle arrest accompanied production secretion proinflammatory molecules (i.e., senescence-associated secretory phenotype [SASP]). Excess senescent cells SASP have deleterious effects on function states CVD, making it putative therapeutic target for improving preventing or reversing CVD. This review will focus role age-related dysfunction We examine established emerging mechanisms underlying senescence-induced dysfunction. then discuss groups impaired high burden strategies reduce remove who are likely benefit most from these therapies. Finally, we highlight systemic suppression other tissues organs, given integrative vasculature physiology. Together, this underscore imperative need deeper understanding translational use targeting therapies burden.

Language: Английский

Studying Werner syndrome to elucidate mechanisms and therapeutics of human aging and age-related diseases DOI
Sofie Lautrup, Domenica Caponio, Hoi‐Hung Cheung

et al.

Biogerontology, Journal Year: 2019, Volume and Issue: 20(3), P. 255 - 269

Published: Jan. 21, 2019

Language: Английский

Citations

30
Supplementation with phosphatidylethanolamine confers anti-oxidant and anti-aging effects via hormesis and reduced insulin/IGF-1-like signaling in C. elegans DOI
Su-Hyeon Park, Bo-Kyoung Kim, Sang-Kyu Park

et al.

Mechanisms of Ageing and Development, Journal Year: 2021, Volume and Issue: 197, P. 111498 - 111498

Published: May 8, 2021

Language: Английский

Citations

26
The Genetic and Epigenetic Arms of Human Ageing and Longevity DOI Creative Commons
Elena Ciaglia, Francesco Montella, Valentina Lopardo

et al.

Biology, Journal Year: 2025, Volume and Issue: 14(1), P. 92 - 92

Published: Jan. 18, 2025

This proposed review aims to shed light on the major genetic and epigenetic contributions ageing process longevity of individuals. In this context, we summarize state knowledge most important variants, their interactions with environment, in achieving a healthy lifespan. We also explore contribution lifestyle influence non-heritable environmental factors (i.e., epigenetics). Accordingly, discuss role inflammageing as one targets overcome morbidity mortality older people for maintenance ageing. more integrated view will display not only underlying mechanisms at play but invites reader rethink both our attitudes toward age.

Language: Английский

Citations

0
It Takes a Village of Chromatin Remodelers to Regulate rDNA Expression DOI Open Access
Mathieu Lévesque, David J. Picketts

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(4), P. 1772 - 1772

Published: Feb. 19, 2025

Ribosome biogenesis is one of the most fundamental and energetically demanding cellular processes. In humans, ribosomal DNA (rDNA) repeats span a large region comprise 200 to 600 copies ~43 kb unit spread over five different chromosomes. Control ribosome closely tied regulation chromatin environment this genomic region. The proportion rDNA loci which are active or silent altered depending on proliferative metabolic state cell. Repeat silencing driven by epigenetic changes culminating in repressive heterochromatin environment. One group proteins facilitating these response growth demands ATP-dependent remodeling protein complexes that use ATP hydrolysis reposition nucleosomes. Indeed, some remodelers known have indispensable roles regulating rDNA. review, we highlight their describe mechanistic at We also introduce developmental disorders arising from dysfunction discuss how consequent dysregulation may be reflected phenotypes observed.

Language: Английский

Citations

0
Mechanisms of cellular senescence-induced vascular aging: evidence of senotherapeutic strategies DOI Open Access
Sophia Mahoney, Samuel I. Bloom,

Douglas R. Seals

et al.

The Journal of Cardiovascular Aging, Journal Year: 2025, Volume and Issue: 5(1)

Published: March 20, 2025

Cardiovascular diseases (CVD) remain the leading cause of death worldwide, with advancing age being primary, nonmodifiable risk factor. Vascular dysfunction, namely arterial stiffening and endothelial is key antecedent to development clinical CVD aging. Fundamental aging macro-mechanistic processes that drive vascular include excess oxidative stress, chronic inflammation, declines in vasodilatory molecule nitric oxide. An important hallmark contributes cellular senescence - a stress response characterized by cell cycle arrest accompanied production secretion proinflammatory molecules (i.e., senescence-associated secretory phenotype [SASP]). Excess senescent cells SASP have deleterious effects on function states CVD, making it putative therapeutic target for improving preventing or reversing CVD. This review will focus role age-related dysfunction We examine established emerging mechanisms underlying senescence-induced dysfunction. then discuss groups impaired high burden strategies reduce remove who are likely benefit most from these therapies. Finally, we highlight systemic suppression other tissues organs, given integrative vasculature physiology. Together, this underscore imperative need deeper understanding translational use targeting therapies burden.

Language: Английский

Citations

0