The Role of Telomeres and Telomerase in Aging

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Cellular Biochemistry".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 175

Special Issue Editor


E-Mail Website
Guest Editor
Institute of Ageing Research, Hangzhou Normal University, Hangzhou 311121, China
Interests: telomere; telomerase; senescence; TELODIN

Special Issue Information

Dear Colleagues,

Telomeres function as a mitotic clock regulating cellular ageing. However, how telomeres regulate ageing remains largely to be elucidated. Recently, there have been many research fronts on telomere biology related to ageing in different model organisms. Although ageing inevitably occurs, premature ageing occurs as the biggest risk factor of chronic diseases. It has been thought that genetic element and environmental stress factors interact precipitating premature ageing. For example, stress may somehow accelerate telomere shortening to set off stem-cell senescence. However, telomeres are synthesised and thereby lengthened by telomerase in stem cells. It is intriguing how telomerase and telomeres may be compromised in premature ageing, thus facilitating age-related diseases.

Ageing occurs in different cell types in various tissues and organs. However, why telomerase may affect some cell types but not others and if controlled expression of telomere binding proteins and their recruiting telomerase might protect the between tissue balance of telomere maintenance in response to diverse stresses. Studies have shown that telomerase expression delays ageing, although telomerase activators have not yet been reported. Intriguingly, a number of biomolecules have been tested in protecting telomeres. These might represent exciting future directions in studying the roles of telomeres and telomerase in ageing, resetting the telomere mitotic clock for stem-cell rejuvenation and prolonged healthspan in epithelial/endothelial cell ageing damage repair, for example.

This Special Issue of the Biomolecules will focus on “The Role of Telomeres and Telomerase in Aging”, including new insights into the molecular and cellular mechanisms of telomere length variations, telomerase structures and other telomere binding proteins, stem cell senescence, and aging-related diseases. Moreover, emerging data on natural or synthetic epigenetic modulators in relation with new molecular targeting options or therapeutic strategies are welcome.

Prof. Dr. Jun-Ping Liu
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers

This special issue is now open for submission.
Back to TopTop