Senescent Cells: Emerging Targets for Human Aging and Age-Related Diseases DOI

Shuling Song,

Eric W.‐F. Lam, Tamar Tchkonia

et al.

Trends in Biochemical Sciences, Journal Year: 2020, Volume and Issue: 45(7), P. 578 - 592

Published: April 6, 2020

Language: Английский

Senescence and Cancer: A Review of Clinical Implications of Senescence and Senotherapies DOI Open Access
Lynda Wyld, Ilaria Bellantuono, Tamar Tchkonia

et al.

Cancers, Journal Year: 2020, Volume and Issue: 12(8), P. 2134 - 2134

Published: July 31, 2020

Cellular senescence is a key component of human aging that can be induced by range stimuli, including DNA damage, cellular stress, telomere shortening, and the activation oncogenes. Senescence generally regarded as tumour suppressive process, both preventing cancer cell proliferation suppressing malignant progression from pre-malignant to disease. It may also effector mechanism many types anticancer therapies, such chemotherapy, radiotherapy, endocrine directly via bioactive molecules released senescent cells stimulate an immune response. However, contribute reduced patient resilience therapies provide pathway for disease recurrence after therapy. A new group drugs, senotherapies, (drugs which interact with interfere their pro-aging impacts either selectively destroying (senolytic drugs) or inhibiting function (senostatic drugs)) are under active investigation determine whether they enhance efficacy improve treatments. Senolytic drugs include quercetin, navitoclax, fisetin preclinical early phase clinical data emerging potential role in treatments, although none yet routine use clinically. This article provides review these issues.

Language: Английский

Citations

187

Mitophagy, Mitochondrial Dynamics, and Homeostasis in Cardiovascular Aging DOI Creative Commons
Ne N. Wu, Yingmei Zhang, Jun Ren

et al.

Oxidative Medicine and Cellular Longevity, Journal Year: 2019, Volume and Issue: 2019, P. 1 - 15

Published: Nov. 4, 2019

Biological aging is an inevitable and independent risk factor for a wide array of chronic diseases including cardiovascular metabolic diseases. Ample evidence has established pivotal role interrupted mitochondrial homeostasis in the onset development aging-related anomalies. A number culprit factors have been suggested aging-associated anomalies oxidative stress, lipid toxicity, telomere shortening, disturbance, DNA damage, with recent findings revealing likely compromised dynamics quality control machinery such as autophagy. Mitochondria undergo consistent fusion fission, which are crucial energy adaptation. Autophagy, particular, mitochondria-selective autophagy, namely, mitophagy, refers to highly conservative cellular process degrade clear long-lived or damaged organelles mitochondria, function gradually deteriorates increased age. Mitochondrial could be achieved through cascade but closely related processes fusion, biogenesis. With improved health care human longevity, ever-rising society imposed high disease prevalence. It thus imperative understand regulation lifespan healthspan. Targeting should offer promising novel therapeutic strategies against complications, particularly

Language: Английский

Citations

171

Making sense of the ageing methylome DOI
Kirsten Seale, Steve Horvath, Andrew E. Teschendorff

et al.

Nature Reviews Genetics, Journal Year: 2022, Volume and Issue: 23(10), P. 585 - 605

Published: May 2, 2022

Language: Английский

Citations

169

Plasma metabolites to profile pathways in noncommunicable disease multimorbidity DOI
Maik Pietzner,

Isobel D. Stewart,

Johannes Raffler

et al.

Nature Medicine, Journal Year: 2021, Volume and Issue: 27(3), P. 471 - 479

Published: March 1, 2021

Language: Английский

Citations

154

Senescent Cells: Emerging Targets for Human Aging and Age-Related Diseases DOI

Shuling Song,

Eric W.‐F. Lam, Tamar Tchkonia

et al.

Trends in Biochemical Sciences, Journal Year: 2020, Volume and Issue: 45(7), P. 578 - 592

Published: April 6, 2020

Language: Английский

Citations

153