{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,3]],"date-time":"2026-07-03T00:48:41Z","timestamp":1783039721456,"version":"3.54.6"},"reference-count":38,"publisher":"Termedia Sp. z.o.o.","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Reumatologia"],"published-print":{"date-parts":[[2017,4,28]]},"abstract":"<jats:p>Inflammatory response is accompanied by changes in cellular energy metabolism. Proinflammatory mediators like plasma C-reactive protein, IL-6, plasminogen activator inhibitor-1, TNF-\uf061 or monocyte chemoattractant protein-1 released in the site of inflammation activates immune cells and increase energy consumption. Increased demand for energy creates local hypoxia and lead in consequence to mitochondrial dysfunction. Metabolism of cells is switched to anaerobic glycolysis. Mitochondria continuously generate free radicals that what result in imbalance that causes oxidative stress, which results in oxidative damage. Chronic energy imbalance promotes oxidative stress, aging, and neurodegeneration and is associated with numerous disorders like Alzheimer\u2019s disease, multiple sclerosis, Parkinson\u2019s disease or Huntington\u2019s disease. It is also believed that oxidative stress and the formation of free radicals play an important role in the pathogenesis of rheumatoid diseases including especially rheumatoid arthritis. Pharmacological control of energy metabolism disturbances may be valuable therapeutic strategy of treatment of this disorders. In recent review we sum up knowledge related to energy disturbances and discuss phenomena such as zombies or hibernation which may indicate the potential targets for regulation of energy metabolism.<\/jats:p>","DOI":"10.5114\/reum.2017.67605","type":"journal-article","created":{"date-parts":[[2017,5,31]],"date-time":"2017-05-31T11:18:55Z","timestamp":1496229535000},"page":"94-99","source":"Crossref","is-referenced-by-count":12,"title":["The human body as an energetic hybrid? New perspectives for chronic disease treatment?"],"prefix":"10.5114","volume":"55","author":[{"given":"Micha\u0142","family":"Gajewski","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Przemys\u0142aw","family":"Rzodkiewicz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S\u0142awomir","family":"Ma\u015bli\u0144ski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"3061","published-online":{"date-parts":[[2017,4,28]]},"reference":[{"key":"ref-795200","doi-asserted-by":"crossref","unstructured":"Straub RH. Evolutionary medicine and chronic inflammatory state-known and new concepts in pathophysiology. J Mol Med (Berl) 2012; 90: 523-534.","DOI":"10.1007\/s00109-012-0861-8"},{"key":"ref-795201","doi-asserted-by":"crossref","unstructured":"Romson JL. 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