scholarly journals Cell aging preserves cellular immortality in the presence of lethal levels of damage

PLoS Biology ◽  
2019 ◽  
Vol 17 (5) ◽  
pp. e3000266 ◽  
Author(s):  
Audrey Menegaz Proenca ◽  
Camilla Ulla Rang ◽  
Andrew Qiu ◽  
Chao Shi ◽  
Lin Chao
2020 ◽  
Author(s):  
Min Ji Han ◽  
Won Ji Lee ◽  
Joonhyuk Choi ◽  
Yean Ju Hong ◽  
Sang Jun Uhm ◽  
...  

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 2116-P
Author(s):  
JEEYEON CHA ◽  
EMILY M. WALKER ◽  
XIN TONG ◽  
MIN GUO ◽  
JIN HUA LIU ◽  
...  

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 667
Author(s):  
Gabriella Racchetti ◽  
Jacopo Meldolesi

Mesenchymal stem cells (MSCs), the cells distributed in the stromas of the body, are known for various properties including replication, the potential of various differentiations, the immune-related processes including inflammation. About two decades ago, these cells were shown to play relevant roles in the therapy of numerous diseases, dependent on their immune regulation and their release of cytokines and growth factors, with ensuing activation of favorable enzymes and processes. Such discovery induced great increase of their investigation. Soon thereafter, however, it became clear that therapeutic actions of MSCs are risky, accompanied by serious drawbacks and defects. MSC therapy has been therefore reduced to a few diseases, replaced for the others by their extracellular vesicles, the MSC-EVs. The latter vesicles recapitulate most therapeutic actions of MSCs, with equal or even better efficacies and without the serious drawbacks of the parent cells. In addition, MSC-EVs are characterized by many advantages, among which are their heterogeneities dependent on the stromas of origin, the alleviation of cell aging, the regulation of immune responses and inflammation. Here we illustrate the MSC-EV therapeutic effects, largely mediated by specific miRNAs, covering various diseases and pathological processes occurring in the bones, heart and vessels, kidney, and brain. MSC-EVs operate also on the development of cancers and on COVID-19, where they alleviate the organ lesions induced by the virus. Therapy by MSC-EVs can be improved by combination of their innate potential to engineering processes inducing precise targeting and transfer of drugs. The unique properties of MSC-EVs explain their intense studies, carried out with extraordinary success. Although not yet developed to clinical practice, the perspectives for proximal future are encouraging.


2021 ◽  
Author(s):  
Maria Mittelbrunn ◽  
Guido Kroemer
Keyword(s):  
T Cell ◽  

1986 ◽  
Vol 159 (1) ◽  
pp. 73-76 ◽  
Author(s):  
Hitoshi Imanishi ◽  
Tetsuro Nakai ◽  
Tatsuo Abe ◽  
Tatsuro Takino

Fly ◽  
2012 ◽  
Vol 6 (2) ◽  
pp. 108-112 ◽  
Author(s):  
Hakima Flici ◽  
Angela Giangrande

Blood ◽  
2003 ◽  
Vol 102 (9) ◽  
pp. 3244-3251 ◽  
Author(s):  
Vladimir Janković ◽  
Ilhem Messaoudi ◽  
Janko Nikolich-Žugich

AbstractA prominent theory of immune senescence holds that repeated antigenic stimulation and decreased production of naive cells combine to progressively exhaust the reserve of lymphocytes available to fight new pathogens, culminating in an accumulation of lymphocytes that achieved replicative senescence. A well-defined primate model of immune senescence in vivo would greatly facilitate testing of this theory. Here, we investigated phenotypic and functional T-cell aging in the rhesus macaques (RMs), currently the dominant primate model of AIDS. Our results show that sharp differences exist between the CD8 and CD4 T-cell subsets in (1) cell-cycle programs (as assessed by both in vitro proliferation and in vivo turnover measurement); (2) CD28 regulation on cell-cycle entry; and (3) accumulation of immediate effector cells among the CD28– cells, believed to be close to or at replicative senescence. These results further suggest poor reliability of CD28 as a marker for senescence. We suggest that some of the T-cell aging phenomenology in RMs can be ascribed to accentuation over time of the inherent differences in activation programs in CD8 and CD4 T cells.


2013 ◽  
Vol 452 (2) ◽  
pp. e1-e2 ◽  
Author(s):  
Michael S. Wolin

Observations by Kozieł et al. reported in this issue of the Biochemical Journal suggest the existence of novel regulatory processes associated with new evidence for increased Nox4 (NAPDH oxidase 4) regulation of mitochondrial function in a cultured endothelial cell aging-induced senescence model. Cellular aging appears to promote a Nox4 interaction with mitochondria that disrupts complex I in the electron transport chain and increases the detection of mitochondrial H2O2. Nox4 appears to maintain a highly interconnected mitochondrial network, which may influence mitochondrial fission and/or fusion mechanisms in a manner that could be a contributing factor in the loss of replicative lifespan seen in senescence.


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