Cell stem cell, Год журнала: 2023, Номер 30(11), С. 1452 - 1471.e10
Опубликована: Окт. 12, 2023
Язык: Английский
Nature Reviews Molecular Cell Biology, Год журнала: 2020, Номер 21(3), С. 137 - 150
Опубликована: Фев. 4, 2020
Язык: Английский
Процитировано
392
Signal Transduction and Targeted Therapy, Год журнала: 2022, Номер 7(1)
Опубликована: Ноя. 7, 2022
Abstract Aging is accompanied by the decline of organismal functions and a series prominent hallmarks, including genetic epigenetic alterations. These aging-associated changes include DNA methylation, histone modification, chromatin remodeling, non-coding RNA (ncRNA) regulation, all which participate in regulation aging process, hence contribute to aging-related diseases. Therefore, understanding mechanisms will provide new avenues develop strategies delay aging. Indeed, interventions based on manipulating have led alleviation or extension lifespan animal models. Small molecule-based therapies reprogramming that enable rejuvenation been developed for ameliorating reversing conditions. In addition, adopting health-promoting activities, such as caloric restriction, exercise, calibrating circadian rhythm, has demonstrated Furthermore, various clinical trials intervention are ongoing, providing more evidence safety efficacy these therapies. Here, we review recent work outline advances age-associated A better critical roles epigenetics process lead prevention human therapy
Язык: Английский
Процитировано
335
Science China Life Sciences, Год журнала: 2022, Номер 65(12), С. 2354 - 2454
Опубликована: Сен. 2, 2022
Язык: Английский
Процитировано
244
Circulation Research, Год журнала: 2018, Номер 123(7), С. 773 - 786
Опубликована: Сен. 13, 2018
Aging is associated with a progressive decline in cardiovascular structure and function. Accumulating evidence links aging to epigenetic alterations encompassing complex interplay of DNA methylation, histone posttranslational modifications, dynamic nucleosome occupancy governed by numerous factors. Advances genomics technology have led profound understanding chromatin reorganization both diseases. This review summarizes recent discoveries mechanisms involved diseases discusses potential therapeutic strategies retard conquer related through the rejuvenation signatures young state.
Язык: Английский
Процитировано
237
Cell, Год журнала: 2023, Номер 186(2), С. 287 - 304.e26
Опубликована: Янв. 1, 2023
Whether and how certain transposable elements with viral origins, such as endogenous retroviruses (ERVs) dormant in our genomes, can become awakened contribute to the aging process is largely unknown. In human senescent cells, we found that HERVK (HML-2), most recently integrated ERVs, are unlocked transcribe genes produce retrovirus-like particles (RVLPs). These RVLPs constitute a transmissible message elicit senescence phenotypes young which be blocked by neutralizing antibodies. The activation of ERVs was also observed organs aged primates mice well tissues serum from elderly. Their repression alleviates cellular tissue degeneration and, some extent, organismal aging. findings indicate resurrection hallmark driving force
Язык: Английский
Процитировано
216
Science China Life Sciences, Год журнала: 2023, Номер 66(5), С. 893 - 1066
Опубликована: Апрель 11, 2023
Язык: Английский
Процитировано
205
Nucleic Acids Research, Год журнала: 2020, Номер 48(19), С. 11083 - 11096
Опубликована: Сен. 23, 2020
Abstract N6-Methyladenosine (m6A) messenger RNA methylation is a well-known epitranscriptional regulatory mechanism affecting central biological processes, but its function in human cellular senescence remains uninvestigated. Here, we found that levels of both m6A and the methyltransferase METTL3 were reduced prematurely senescent mesenchymal stem cell (hMSC) models progeroid syndromes. Transcriptional profiling modifications further identified MIS12, for which hMSCs METTL3-deficient hMSCs. Knockout accelerated hMSC whereas overexpression rescued phenotypes. Mechanistically, loss turnover decreased expression MIS12 mRNA while knockout senescence. Furthermore, reader IGF2BP2 was as key player recognizing stabilizing m6A-modified mRNA. Taken together, discovered alleviates through modification-dependent stabilization transcript, representing novel premature
Язык: Английский
Процитировано
142
Science Translational Medicine, Год журнала: 2021, Номер 13(575)
Опубликована: Янв. 6, 2021
Inactivation of the histone acetyltransferase gene KAT7 prolongs survival in naturally aged mice and progeroid that age prematurely.
Язык: Английский
Процитировано
119
Nucleic Acids Research, Год журнала: 2021, Номер 49(8), С. 4203 - 4219
Опубликована: Март 1, 2021
Sirtuin 3 (SIRT3) is an NAD+-dependent deacetylase linked to a broad range of physiological and pathological processes, including aging aging-related diseases. However, the role SIRT3 in regulating human stem cell homeostasis remains unclear. Here we found that expression was downregulated senescent mesenchymal cells (hMSCs). CRISPR/Cas9-mediated depletion led compromised nuclear integrity, loss heterochromatin accelerated senescence hMSCs. Further analysis indicated interacted with envelope proteins heterochromatin-associated proteins. deficiency resulted detachment genomic lamina-associated domains (LADs) from lamina, increased chromatin accessibility aberrant repetitive sequence transcription. The re-introduction rescued disorganized phenotypes. Taken together, our study reveals novel for stabilizing counteracting hMSC senescence, providing new potential therapeutic targets ameliorate
Язык: Английский
Процитировано
117
Cell Discovery, Год журнала: 2022, Номер 8(1)
Опубликована: Фев. 1, 2022
Regenerative capacity declines throughout evolution and with age. In this study, we asked whether metabolic programs underlying regenerative capability might be conserved across species, if so, such drivers harnessed to promote tissue repair. To end, conducted metabolomic analyses in two vertebrate organ regeneration models: the axolotl limb blastema antler stem cells. further reveal why young individuals have higher than elderly, also constructed profiles for primate juvenile aged tissues, as well human joint analyses, uncovered that active pyrimidine metabolism fatty acid correlated capacity. Furthermore, identified a set of regeneration-related metabolite effectors species. One is uridine, nucleoside, which can rejuvenate cells various tissues vivo. These observations will open new avenues intervention repair regeneration.
Язык: Английский
Процитировано
92