@article{KamranfarXueTohgeetal.2018,
  author    = {Kamranfar, Iman and Xue, Gang-Ping and Tohge, Takayuki and Sedaghatmehr, Mastoureh and Fernie, Alisdair R. and Balazadeh, Salma and Mueller-Roeber, Bernd},
  title     = {Transcription factor RD26 is a key regulator of metabolic reprogramming during dark-induced senescence},
  series = {New phytologist : international journal of plant science},
  volume    = {218},
  journal   = {New phytologist : international journal of plant science},
  number    = {4},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {0028-646X},
  doi       = {10.1111/nph.15127},
  pages     = {1543 -- 1557},
  year      = {2018},
  abstract  = {Leaf senescence is a key process in plants that culminates in the degradation of cellular constituents and massive reprogramming of metabolism for the recovery of nutrients from aged leaves for their reuse in newly developing sinks. We used molecular-biological and metabolomics approaches to identify NAC transcription factor (TF) RD26 as an important regulator of metabolic reprogramming in Arabidopsis thaliana. RD26 directly activates CHLOROPLAST VESICULATION (CV), encoding a protein crucial for chloroplast protein degradation, concomitant with an enhanced protein loss in RD26 over-expressors during senescence, but a reduced decline of protein in rd26 knockout mutants. RD26 also directly activates LKR/SDH involved in lysine catabolism, and PES1 important for phytol degradation. Metabolic profiling revealed reduced c-aminobutyric acid (GABA) in RD26 overexpressors, accompanied by the induction of respective catabolic genes. Degradation of lysine, phytol and GABA is instrumental for maintaining mitochondrial respiration in carbon-limiting conditions during senescence. RD26 also supports the degradation of starch and the accumulation of mono-and disaccharides during senescence by directly enhancing the expression of AMY1, SFP1 and SWEET15 involved in carbohydrate metabolism and transport. Collectively, during senescence RD26 acts by controlling the expression of genes across the entire spectrum of the cellular degradation hierarchy.},
  language  = {en}
}
@misc{SadowskaHausmannWuertzKozak2018,
  author    = {Sadowska, Aleksandra and Hausmann, Oliver Nic and Wuertz-Kozak, Karin},
  title     = {Inflammaging in the intervertebral disc},
  series = {Postprints der Universit{\"a}t Potsdam : Mathematisch Naturwissenschaftliche Reihe},
  journal   = {Postprints der Universit{\"a}t Potsdam : Mathematisch Naturwissenschaftliche Reihe},
  number    = {519},
  doi       = {10.25932/publishup-41408},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-414081},
  pages     = {9},
  year      = {2018},
  abstract  = {Degeneration of the intervertebral disc - triggered by ageing, mechanical stress, traumatic injury, infection, inflammation and other factors - has a significant role in the development of low back pain. Back pain not only has a high prevalence, but also a major socio-economic impact. With the ageing population, its occurrence and costs are expected to grow even more in the future. Disc degeneration is characterized by matrix breakdown, loss in proteoglycans and thus water content, disc height loss and an increase in inflammatory molecules. The accumulation of cytokines, such as interleukin (IL)-1 , IL-8 or tumor necrosis factor (TNF)-, together with age-related immune deficiency, leads to the so-called inflammaging - low-grade, chronic inflammation with a crucial role in pain development. Despite the relevance of these molecular processes, current therapies target symptoms, but not underlying causes. This review describes the biological and biomechanical changes that occur in a degenerated disc, discusses the connection between disc degeneration and inflammaging, highlights factors that enhance the inflammatory processes in disc pathologies and suggests future research avenues.},
  language  = {en}
}
@article{BoginVareaHermanussenetal.2018,
  author    = {Bogin, Barry and Varea, Carlos and Hermanussen, Michael and Scheffler, Christiane},
  title     = {Human life course biology},
  series = {American journal of physical anthropology},
  volume    = {165},
  journal   = {American journal of physical anthropology},
  number    = {4},
  publisher = {Wiley},
  address   = {Hoboken},
  issn      = {0002-9483},
  doi       = {10.1002/ajpa.23357},
  pages     = {834 -- 854},
  year      = {2018},
  language  = {en}
}