Antero Salminen - University of Eastern Finland

Molecular Basis of Aging and Alzheimer’s Disease

Antero Salminen

PhD, Research Director, Emeritus

University of Eastern Finland
Institute of Clinical Medicine / Neurology
P.O. Box 1627
FI-70211 Kuopio
Finland
+358-(0)50 574 07 40
e-mail: antero.salminen (at) uef.fi

Major Positions and Appointments

Research Associate	Academy of Finland	1982-1985
Junior Research Fellow	Academy of Finland	1987-1990
Senior Research Fellow	Academy of Finland	1992-1993
Professor of Cell Biology	University of Jyväskylä	1993-1995
Research Director	University of Eastern Finland	1995-2014
Research Director Emeritus	University of Eastern Finland	2014-

Visiting Scientist:

University of California	Berkeley	1986-1987
National Cancer Institute	NIH, Bethesda	1987-1989
University of Hamburg	Medical School, Hamburg	1990-1992
Baylor College of Medicine	Houston	1993

Statistics

(Scopus)

Articles: 253

Citations: 19,085

h-index: 76

Research Interests

NF-κB signaling and inflammaging
Inflammaging stimulates a compensatory immunosuppression which enhances immunosenescence and immune aging
Age-related immunosuppression promotes cellular senescence and tissue degeneration
Aryl hydrocarbon receptor promotes immunosuppression, the aging process, and Alzheimer’s disease
Tissue fibroblasts regulate the aging process in cooperation with the immunosuppressive network

Recent Review Articles

AGING PROCESS

Salminen A. (2024) AMPK signaling inhibits the differentiation of myofibroblasts: impact on age-related tissue fibrosis and degeneration. Biogerontology. https://doi.org/10.1007/s10522-023-10072-9

Salminen A. (2023) The role of immunosuppressive myofibroblasts in the aging process and age-related diseases. J. Mol. Med. (Berl.) 101, 1169-1189. https://doi.org/10.1007/s00109-023-02360-1

Salminen A. (2023) The plasticity of fibroblasts: A forgotten player in the aging process. Ageing Res. Rev. 89,101995. https://doi.org/10.1016/j.arr.2023.101995

Salminen A. (2023) Aryl hydrocarbon receptor (AhR) impairs circadian regulation: Impact on the aging process. Ageing Res. Rev. 87, 101928. https://doi.org/10.1016/j.arr.2023.101928

Salminen A. (2022) Aryl hydrocarbon receptor (AhR) reveals evidence of antagonistic pleiotropy in the regulation of the aging process. Cell. Mol. Life Sci. 79, 489. https://doi.org/10.1007/s00018-022-04520-x

Salminen A. (2022) Mutual antagonism between aryl hydrocarbon receptor and hypoxia-inducible factor-1α (AhR/HIF-1α) signaling: Impact on the aging process. Cell. Signal. 99, 110445. https://doi.org/10.1016/j.cellsig.2022.110445

Salminen A. (2022) Clinical perspectives on the age-related increase of immunosuppressive activity. J. Mol. Med. (Berl) 100, 697-712. https://doi.org/10.1007/s00109-022-02193-4

Salminen A, Kaarniranta K, Kauppinen A. (2022) Photoaging: UV radiation-induced inflammation and immunosuppression accelerate the aging process in the skin. Inflamm. Res. 71, 817-831. https://doi.org/10.1007/s00011-022-01598-8

Salminen A. (2022) Role of indoleamine 2,3-dioxygenase 1 (IDO1) and kynurenine pathway in the regulation of the aging process. Ageing Res. Rev. 75, 101573. https://doi.org/10.1016/j.arr.2022.101573

Salminen A, Kaarniranta K, Kauppinen A. (2021) Insulin/IGF-1 signaling promotes immunosuppression via the STAT3 pathway: impact on the aging process and age-related diseases. Inflamm. Res. 70, 1043-1061. https://doi.org/10.1007/s00011-021-01498-3

Salminen A. (2021) Immunosuppressive network promotes immunosenescence associated with aging and chronic inflammatory conditions. J. Mol. Med. (Berl). 99, 1553-1569. https://doi.org/10.1007/s00109-021-02123-w

Salminen A. (2021) Feed-forward regulation between cellular senescence and immunosuppression promotes the aging process and age-related diseases. Ageing Res. Rev. 67, 101280. https://doi.org/10.1016/j.arr.2021.101280

Salminen A. (2021) Increased immunosuppression impairs tissue homeostasis with aging and age-related diseases. J. Mol. Med. (Berl) 99, 1-20. https://doi.org/10.1007/s00109-020-01988-7

Salminen A. (2020) Activation of immunosuppressive network in the aging process. Ageing Res. Rev. 57, 100998. https://doi.org/10.1016/j.arr.2019.100998

Salminen A, Kaarniranta K, Kauppinen A. (2020) Exosomal vesicles enhance immunosuppression in chronic inflammation: Impact in cellular senescence and the aging process. Cell. Signal. 75, 109771. https://doi.org/10.1016/j.cellsig.2020.109771

Salminen A, Kauppinen A, Kaarniranta K. (2019) AMPK activation inhibits the functions of myeloid-derived suppressor cells (MDSC): impact on cancer and aging. J. Mol. Med. (Berl) 97, 1049-1064. https://doi.org/10.1007/s00109-019-01795-9

Salminen A, Kaarniranta K, Kauppinen A. (2019) Immunosenescence: the potential role of myeloid-derived suppressor cells (MDSC) in age-related immune deficiency. Cell. Mol. Life Sci. 76, 1901-1918. https://doi.org/10.1007/s00018-019-03048-x

Salminen A, Kaarniranta K, Kauppinen A. (2018) The role of myeloid-derived suppressor cells (MDSC) in the inflammaging process. Ageing Res. Rev. 48, 1-10. https://doi.org/10.1016/j.arr.2018.09.001

Salminen A, Kauppinen A, Kaarniranta K. (2018) Myeloid-derived suppressor cells (MDSC): an important partner in cellular/tissue senescence. Biogerontology 19, 325-339. https://doi.org/10.1007/s10522-018-9762-8

Salminen A, Kaarniranta K, Kauppinen A. (2018) Phytochemicals inhibit the immunosuppressive functions of myeloid-derived suppressor cells (MDSC): impact on cancer and age-related chronic inflammatory disorders. Int. Immunopharmacol. 61, 231-240. https://doi.org/10.1016/j.intimp.2018.06.005

Salminen A, Kaarniranta K, Kauppinen A. (2017) Integrated stress response stimulates FGF21 expression: systemic enhancer of longevity. Cell. Signal. 40, 10-21. https://doi.org/10.1016/j.cellsig.2017.08.009

Salminen A, Kaarniranta K, Kauppinen A. (2017) Regulation of longevity by FGF21: interaction between energy metabolism and stress responses. Ageing Res. Rev. 37, 79–93. https://doi.org/10.1016/j.arr.2017.05.004

Salminen A., Kauppinen A., Kaarniranta K. (2017) FGF21 activates AMPK signaling: impact on metabolic regulation and the aging process. J. Mol. Med. (Berl) 95, 123-131. https://doi.org/10.1007/s00109-016-1477-1

Salminen A, Kaarniranta K, Kauppinen A. (2016) Age-related changes in AMPK activation: role for AMPK phosphatases and inhibitory phosphorylation by upstream signaling pathways. Ageing Res. Rev. 28, 15-26. https://doi.org/10.1016/j.arr.2016.04.003

Salminen A, Kaarniranta K, Kauppinen A. (2016) Hypoxia-inducible histone lysine demethylases: impact on the aging process and age-related diseases. Aging Dis. 7, 180-200. https://doi.org/10.14336/AD.2015.0929

Salminen A, Kauppinen A, Kaarniranta K. (2016) AMPK/Snf1 signaling regulates histone acetylation: impact on gene expression and epigenetic functions. Cell. Signal. 28, 887-895. https://doi.org/10.1016/j.cellsig.2016.03.009

Salminen A, Kaarniranta K, Kauppinen A. (2016) AMPK and HIF signaling pathways regulate both longevity and cancer growth: the good news and the bad news about survival mechanisms. Biogerontology 17, 655-680. https://doi.org/10.1007/s10522-016-9655-7

ALZHEIMER’S DISEASE

Salminen A. (2023) Activation of aryl hydrocarbon receptor (AhR) in Alzheimer's disease: role of tryptophan metabolites generated by gut host-microbiota. J. Mol. Med. (Berl) 101, 201-222. https://doi.org/10.1007/s00109-023-02289-5

Salminen A, Kaarniranta K, Kauppinen A. (2021) Hypoxia/ischemia impairs CD33 (Siglec-3) /TREM2 signaling: Potential role in Alzheimer's pathogenesis. Neurochem. Int. 150, 105186. https://doi.org/10.1016/j.neuint.2021.105186

Salminen A. (2021) Hypoperfusion is a potential inducer of immunosuppressive network in Alzheimer’s disease. Neurochem. Int. 142, 104919. https://doi.org/10.1016/j.neuint.2020.104919

Salminen A, Kaarniranta K, Kauppinen A. (2020) ER stress activates immunosuppressive network: implications for aging and Alzheimer’s disease. J. Mol. Med. (Berl) 98, 633-650. https://doi.org/10.1007/s00109-020-01904-z

Salminen A, Kaarniranta K, Kauppinen A. (2018) The potential importance of myeloid-derived suppressor cells (MDSCs) in the pathogenesis of Alzheimer’s disease. Cell. Mol. Life Sci. 75, 3099-3120. https://doi.org/10.1007/s00018-018-2844-6

Salminen A, Kauppinen A, Kaarniranta K. (2017) Hypoxia/ischemia activate processing of Amyloid Precursor Protein: impact of vascular dysfunction in the pathogenesis of Alzheimer’s disease. J. Neurochem. 140, 536-549. https://doi.org/10.1111/jnc.13932

Salminen A, Jouhten P, Sarajärvi T, Haapasalo A, Hiltunen M. (2016) Hypoxia and GABA shunt activation in the pathogenesis of Alzheimer’s disease. Neurochem. Int. 92, 13-24. https://doi.org/10.1016/j.neuint.2015.11.005

AGE-RELATED MACULAR DEGENERATION (AMD)

Kauppinen A, Kaarniranta K, Salminen A. (2020) Potential role of myeloid-derived suppressor cells (MDSCs) in age-related macular degeneration (AMD). Front. Immunol. 11, 384. https://doi.org/10.3389/fimmu.2020.00384

Kaarniranta K, Uusitalo H, Blasiak J, Felszeghy S, Kannan R, Kauppinen A, Salminen A, Sinha D, Ferrington D. (2020) Mechanisms of mitochondrial dysfunction and their impact on age-related macular degeneration. Prog. Retin. Eye Res. 79, 100858. https://doi.org/10.1016/j.preteyeres.2020.100858

Hyttinen JMT, Kannan R, Felszeghy S, Niittykoski M, Salminen A, Kaarniranta K. (2019) The regulation of NFE2L2 (NRF2) signalling and epithelial-to-mesenchymal transition in age-related macular degeneration pathology. Int. J. Mol. Sci. 20, 5800. https://doi.org/10.3390/ijms20225800

Kaarniranta K, Koskela A, Felszeghy S, Kivinen N, Salminen A, Kauppinen A. (2019) Fatty acids and oxidized lipoproteins contribute to autophagy and innate immunity responses upon the degeneration of retinal pigment epithelium and development of age-related macular degeneration. Biochimie 159, 49-54. https://doi.org/10.1016/j.biochi.2018.07.010

Hyttinen JM, Blasiak J, Niittykoski M, Kinnunen K, Kauppinen A, Salminen A, Kaarniranta K. (2017) DNA damage response and autophagy in the degeneration of retinal pigment epithelial cells: implications for age-related macular degeneration (AMD). Ageing Res. Rev. 36, 64-77. https://doi.org/10.1016/j.arr.2017.03.006