Journal ArticleDOI
Keeping zombies alive: The ER-mitochondria Ca2+ transfer in cellular senescence
Ulises Ahumada-Castro,Andrea Puebla-Huerta,Victor Cuevas-Espinoza,Alenka Lovy,J. Cesar Cardenas +4 more
TLDR
In this paper, the possible connection between endoplasmic reticulum (ER) and mitochondria Ca2+ transfer and senescence is reviewed, where the authors identify new therapeutic targets that allow either delaying senescent cell accumulation or reducing senescent cells burden to alleviate multiple diseases.About:
This article is published in Biochimica et Biophysica Acta.The article was published on 2021-10-01. It has received 16 citations till now. The article focuses on the topics: Senescence & Mitochondrion.read more
Citations
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The Mitochondrial-Associated Endoplasmic Reticulum Membrane and Its Role in Diabetic Nephropathy.
Lihua Ni,Cheng Yuan +1 more
TL;DR: The mitochondrial-associated endoplasmic reticulum membrane (MAM) as discussed by the authors was found to be involved in a wide range of cellular functions, such as calcium signaling, the division and fusion of mitochondria, and the synthesis and transport of lipids.
Journal ArticleDOI
The relevance of organelle interactions in cellular senescence
TL;DR: The role of organelle interactions in cellular senescence is summarized, their relevance for cellular calcium homeostasis, protein and lipid homeostases, and mitochondrial quality control is highlighted, and important clues for intervention strategies from a new perspective are provided.
Journal ArticleDOI
Aorta- and liver-generated TMAO enhances trained immunity for increased inflammation via ER stress/mitochondrial ROS/glycolysis pathways
Fatma Saaoud,Lu-ran Liu,Keman Xu,Ramon Cueto,Ying Shao,Yifan Lu,Yu Sun,Nathaniel W. Snyder,Sheng-Chang Wu,Ling Yang,Yan Zhou,David R. Williams,Chuanfu Li,Laisel Martinez,Roberto I. Vazquez-Padron,Huaqing Zhao,Xiaohua Jiang,Hong Wang,Xiaofeng Yang +18 more
TL;DR: In this paper , the authors determined whether TMA is oxidized into trimethylamine N-oxide (TMAO) in nonliver tissues and whether it promotes inflammation via trained immunity.
Journal ArticleDOI
Modulation of Oxidative Stress-Induced Senescence during Non-Alcoholic Fatty Liver Disease
TL;DR: The modulation of cellular senescence can be beneficial to ameliorate oxidative stress-related damage during NAFLD progression and the possibilities to modulate senescences as a therapeutic strategy in the treatment of NAFLd are discussed.
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Targeting mitochondria in dermatological therapy: beyond oxidative damage and skin aging
TL;DR: The functions of mitochondria in cutaneous physiology beyond energy (ATP) and ROS production are examined and the mitochondrial protein MPZL3 as a promising new drug target for future ‘mitochondrial dermatology’ is highlighted.
References
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Journal ArticleDOI
The serial cultivation of human diploid cell strains.
Leonard Hayflick,P.S. Moorhead +1 more
TL;DR: A consideration of the cause of the eventual degeneration of these strains leads to the hypothesis that non-cumulative external factors are excluded and that the phenomenon is attributable to intrinsic factors which are expressed as senescence at the cellular level.
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A biomarker that identifies senescent human cells in culture and in aging skin in vivo
Goberdhan P. Dimri,X Lee,G Basile,Meileen Acosta,G Scott,C Roskelley,E E Medrano,Maarten H.K. Linskens,Ivica Rubelj,Olivia M. Pereira-Smith +9 more
TL;DR: It is shown that several human cells express a beta-galactosidase, histochemically detectable at pH 6, upon senescence in culture, which provides in situ evidence that senescent cells may exist and accumulate with age in vivo.
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The Senescence-Associated Secretory Phenotype: The Dark Side of Tumor Suppression
TL;DR: A senescence-associated secretory phenotype (SASP) is acquired that turns senescent fibroblasts into proinflammatory cells that have the ability to promote tumor progression.
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Clearance of p16 Ink4a -positive senescent cells delays ageing-associated disorders
Darren J. Baker,Tobias Wijshake,Tamar Tchkonia,Nathan K. LeBrasseur,Bennett G. Childs,Bart van de Sluis,James L. Kirkland,Jan M. van Deursen +7 more
TL;DR: Data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.