Grundlagen der biologischen Alterung

Schosserer, Markus; Grubeck‐Loebenstein, B.; Grillari, Johannes

doi:10.1007/s00391-015-0857-4

Cited by 10 publications

(3 citation statements)

References 32 publications

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“…In many tissues, aging has been known to induce cell senescence [ 39 , 40 ], which deter wound healing [ 41 ]. Our recent study on an animal model found that the expression of CCN-1, a senescent protein, in TSCs increased in an age-depended manner [ 32 ].…”

Section: Discussionmentioning

confidence: 99%

Moderate treadmill running exercise prior to tendon injury enhances wound healing in aging rats

2016

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The effect of exercise on wound healing in aging tendon was tested using a rat moderate treadmill running (MTR) model. The rats were divided into an MTR group that ran on a treadmill for 4 weeks and a control group that remained in cages. After MTR, a window defect was created in the patellar tendons of all rats and wound healing was analyzed. We found that MTR accelerated wound healing by promoting quicker closure of wounds, improving the organization of collagen fibers, and decreasing senescent cells in the wounded tendons when compared to the cage control. MTR also lowered vascularization, increased the numbers of tendon stem/progenitor cells (TSCs) and TSC proliferation than the control. Besides, MTR significantly increased the expression of stem cell markers, OCT-4 and Nanog, and tenocyte genes, Collagen I, Collagen III and tenomodulin, and down-regulated PPAR-γ, Collagen II and Runx-2 (non-tenocyte genes). These findings indicated that moderate exercise enhances healing of injuries in aging tendons through TSC based mechanisms, through which exercise regulates beneficial effects in tendons. This study reveals that appropriate exercise may be used in clinics to enhance tendon healing in aging patients.

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Section: Discussionmentioning

confidence: 99%

Moderate treadmill running exercise prior to tendon injury enhances wound healing in aging rats

2016

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“…The accumulation of senescent cells has been demonstrated during organism aging [ 19 ], which suggests that senescent cells may play a role in aging-associated disease, including prostate cancer. Cellular senescence seems to exhibit diverse effects on epithelial and stromal cells in prostate cancer [ 20 , 21 ].…”

Section: Discussionmentioning

confidence: 99%

Ginsenoside Rg3 inhibits the senescence of prostate stromal cells through down-regulation of interleukin 8 expression

et al. 2017

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Senescent stromal cells support the development of prostate cancer and are considered potential therapeutic targets. This research evaluated the regulatory effects of ginsenoside Rg3 on the senescence of prostatic stromal cells pre-incubated in medium supplemented with 0.5% fetal bovine serum. The results revealed that ginsenoside Rg3 decreased the number of stromal cells positively stained with a senescent cell marker (senescence-associated β-galactosidase). Ginsenoside Rg3 also increased the viability of stromal cells and promoted cell cycle transition from G0/G1 to S phase, as well as inhibited the carcinoma-associated fibroblast-like phenotype in prostate stromal cells, through the up-regulation of smooth muscle cell markers SM22 and smooth muscle myosin heavy chain. Conditioned medium collected from stromal cells treated with ginsenoside Rg3 exhibited an attenuated effect on the promotion of prostate cancer cell migration compared with conditioned medium from stromal cells without Rg3 treatment. Down-regulation of interleukin 8 (IL-8) in a dose- and time-dependent manner was observed in ginsenoside Rg3-treated stromal cells, and over-expression or addition of IL-8 reversed the anti-senescence role of Rg3 in prostate stromal cells. Furthermore, ginsenoside Rg3 down-regulated IL-8 expression by decreasing the reactive oxygen species level in prostatic stromal cells and reducing the transcriptional activity of IL-8 promoter by damping the transcription factors C/EBP β and p65 binding to IL-8 promoter. Our research revealed that ginsenoside Rg3 was able to inhibit prostate stromal cell senescence by down-regulating IL-8 expression. The results suggest a potential value for ginsenoside Rg3 in prostate cancer treatment through the targeting of pro-carcinogenic senescent stromal cells.

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“…Alterung ist ein vorwiegend linearer kataboler Prozess, welcher die Vulnerabilität für die Entwicklung altersabhängiger akuter oder chronischer Erkrankungen z. T. wesentlich fördert 6 . Eine häufig bereits bestehende Vulnerabilität der molekularen Zellordnung wird zusätzlich durch chronischen Stress erheblich verstärkt, was den biologischen Altersprozess z. T. deutlich akzeleriert, dokumentiert durch Zunahme biologischer Altersmarker und degenerativer Erkrankungen 16 . Langlebigkeit wiederum wird durch intakte spezifische Aktivität der zellulären Stressresistenz und Reparatursysteme (z.…”

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Stress und Alterung

Wolf¹

2022

Zeitschrift für Orthomolekulare Medizin

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ZusammenfassungDer biologische Alterungsprozess besteht aus Änderungen von molekularen Strukturen und deren Funktionen bei unzureichenden Reparaturmechanismen. Dieser katabole Prozess fördert die Vulnerabilität für altersabhängige Erkrankungen wie degenerative Gehirnerkrankungen. Verstärkend wirken dabei chronischer Stress, psychische Belastung, Genetik/Epigenetik, endokrine Alterung und bestimmte Lebensstilfaktoren. Dauerhaft verstärkte Stressexposition verändert den gesamten Zellstoffwechsel und erhöht dadurch das Risiko für den Verlust von physischer und emotionaler Lebensqualität, organischer Gesamtfunktion und Mortalität.

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Grundlagen der biologischen Alterung

Cited by 10 publications

References 32 publications

Moderate treadmill running exercise prior to tendon injury enhances wound healing in aging rats

Moderate treadmill running exercise prior to tendon injury enhances wound healing in aging rats

Ginsenoside Rg3 inhibits the senescence of prostate stromal cells through down-regulation of interleukin 8 expression

Stress und Alterung

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