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Anu Kauppinen

Researcher at University of Eastern Finland

Publications -  130
Citations -  10079

Anu Kauppinen is an academic researcher from University of Eastern Finland. The author has contributed to research in topics: Inflammation & Autophagy. The author has an hindex of 44, co-authored 115 publications receiving 7325 citations. Previous affiliations of Anu Kauppinen include Oulu University Hospital.

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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

Daniel J. Klionsky, +2983 more
- 08 Feb 2021 - 
TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.
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Antagonistic crosstalk between NF-κB and SIRT1 in the regulation of inflammation and metabolic disorders.

TL;DR: The molecular mechanisms of the antagonistic signaling between NF-κB and SIRT1 are examined and how this crosstalk controls inflammatory process and energy metabolism is described to induce the appearance of chronic inflammation in metabolic diseases.
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Emerging role of NF-κB signaling in the induction of senescence-associated secretory phenotype (SASP).

TL;DR: The major hallmark of cellular senescence is an irreversible cell cycle arrest and thus it is a potent tumor suppressor mechanism and emerging data has revealed that NF-κB signaling is the major signaling pathway which stimulates the appearance of SASP.
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Activation of innate immunity system during aging: NF-kB signaling is the molecular culprit of inflamm-aging.

TL;DR: The conclusion is that NF-kB signaling seems to be the culprit of inflamm-aging, since this signaling system integrates the intracellular regulation of immune responses in both aging and age-related diseases.
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Inflammation and its role in age-related macular degeneration

TL;DR: Elevations in levels of local and systemic biomarkers indicate that chronic inflammation is involved in the pathogenesis of both disease forms of age-related macular degeneration.