Molecular mechanisms of environmental pollutant-induced cartilage damage: from developmental disorders to osteoarthritis.

Autor: Skalny AV; IM Sechenov First Moscow State Medical University (Sechenov University), 119435, Moscow, Russia., Aschner M; Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY, 10461, USA., Zhang F; Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Health Science Center, School of Public Health, Xi'an Jiaotong University, Xi'an, 710061, China., Guo X; Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Health Science Center, School of Public Health, Xi'an Jiaotong University, Xi'an, 710061, China., Buha Djordevic A; Department of Toxicology 'Akademik Danilo Soldatović', Faculty of Pharmacy, University of Belgrade, 11000, Belgrade, Serbia., Sotnikova TI; IM Sechenov First Moscow State Medical University (Sechenov University), 119435, Moscow, Russia.; City Clinical Hospital N. a. S.P. Botkin of the Moscow City Health Department, 125284, Moscow, Russia., Korobeinikova TV; IM Sechenov First Moscow State Medical University (Sechenov University), 119435, Moscow, Russia., Domingo JL; Laboratory of Toxicology and Environmental Health, School of Medicine, Universitat Rovira I Virgili, 4320, Reus, Catalonia, Spain., Farsky SHP; Department of Clinical and Toxicological Analyses, Faculty of Pharmaceutical Sciences, University of São Paulo, São Paulo, SP, 005508-000, Brazil., Tinkov AA; IM Sechenov First Moscow State Medical University (Sechenov University), 119435, Moscow, Russia. tinkov.a.a@gmail.com.; Laboratory of Ecobiomonitoring and Quality Control, Yaroslavl State University, 150003, Yaroslavl, Russia. tinkov.a.a@gmail.com.
Jazyk: angličtina
Zdroj: Archives of toxicology [Arch Toxicol] 2024 Sep; Vol. 98 (9), pp. 2763-2796. Date of Electronic Publication: 2024 May 17.
DOI: 10.1007/s00204-024-03772-9
Abstrakt: The objective of the present study was to review the molecular mechanisms of the adverse effects of environmental pollutants on chondrocytes and extracellular matrix (ECM). Existing data demonstrate that both heavy metals, including cadmium (Cd), lead (Pb), and arsenic (As), as well as organic pollutants, including polychlorinated dioxins and furans (PCDD/Fs) and polychlorinated biphenyls (PCB), bisphenol A, phthalates, polycyclic aromatic hydrocarbons (PAH), pesticides, and certain other organic pollutants that target cartilage ontogeny and functioning. Overall, environmental pollutants reduce chondrocyte viability through the induction apoptosis, senescence, and inflammatory response, resulting in cell death and impaired ECM production. The effects of organic pollutants on chondrocyte development and viability were shown to be mediated by binding to the aryl hydrocarbon receptor (AhR) signaling and modulation of non-coding RNA expression. Adverse effects of pollutant exposures were observed in articular and growth plate chondrocytes. These mechanisms also damage chondrocyte precursors and subsequently hinder cartilage development. In addition, pollutant exposure was shown to impair chondrogenesis by inhibiting the expression of Sox9 and other regulators. Along with altered Runx2 signaling, these effects also contribute to impaired chondrocyte hypertrophy and chondrocyte-to-osteoblast trans-differentiation, resulting in altered endochondral ossification. Several organic pollutants including PCDD/Fs, PCBs and PAHs, were shown to induce transgenerational adverse effects on cartilage development and the resulting skeletal deformities. Despite of epidemiological evidence linking human environmental pollutant exposure to osteoarthritis or other cartilage pathologies, the data on the molecular mechanisms of adverse effects of environmental pollutant exposure on cartilage tissue were obtained from studies in laboratory rodents, fish, or cell cultures and should be carefully extrapolated to humans, although they clearly demonstrate that cartilage should be considered a putative target for environmental pollutant toxicity.
(© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
Databáze: MEDLINE
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