{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T15:35:47Z","timestamp":1784043347547,"version":"3.55.0"},"reference-count":50,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2017,9,12]],"date-time":"2017-09-12T00:00:00Z","timestamp":1505174400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100006143","name":"Department of Science and Technology, Government of Kerala","doi-asserted-by":"publisher","award":["F.No. SB\/SO\/HS\u2010148\/2013"],"award-info":[{"award-number":["F.No. SB\/SO\/HS\u2010148\/2013"]}],"id":[{"id":"10.13039\/501100006143","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001407","name":"Department of Biotechnology, Ministry of Science and Technology, India","doi-asserted-by":"publisher","award":["BT\/PR3709\/BRB\/10\/980\/2011"],"award-info":[{"award-number":["BT\/PR3709\/BRB\/10\/980\/2011"]}],"id":[{"id":"10.13039\/501100001407","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2018,2]]},"abstract":"<jats:sec><jats:label\/><jats:p>Pathological hypertrophy and myocardial infarction (MI) are two etiologically different cardiac disorders having differential molecular mechanisms of disease manifestation. However, no study has been conducted so far to analyze and compare the differential status of energy metabolism in these two disease forms. It was shown recently by our group that production of ATP is significantly impaired during MI along with inhibition of pyruvate dehydrogenase E1\u2010\u03b2 (PDHE1 B) by pyruvate dehydrogenase kinase 4 (PDK4). However, the ATP levels showed no significant change during pathological hypertrophy compared to control group. To seek a plausible explanation of this phenomenon, the peroxisome proliferator\u2010activated receptor alpha (PPAR) pathway was studied in all the experimental groups which revealed that PGC1\u03b1\u2010 ERR\u03b1 axis remains active in MI while the same remained inactive during pathological hypertrophy possibly by NF\u2010\u03baB that plays a significant role in deactivating this pathway during hypertrophy. At the same time, it was observed that reactive oxygen species (ROS) negatively regulates NF\u2010\u03baB activity during MI by oxidation of cysteine residues of p50\u2010 the DNA binding subunit of NF\u2010\u03baB. Thus, this study reports for the first time, a possible mechanism for the differential status of energy metabolism during two etiologically different cardiac pathophysiological conditions involving PGC1\u03b1\u2010ERR\u03b1 axis along with p50 subunit of NF\u2010\u03baB.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.26318","type":"journal-article","created":{"date-parts":[[2017,8,3]],"date-time":"2017-08-03T16:09:03Z","timestamp":1501776543000},"page":"1575-1590","source":"Crossref","is-referenced-by-count":14,"title":["Modulation of NFKB1\/p50 by ROS leads to impaired ATP production during MI compared to cardiac hypertrophy"],"prefix":"10.1002","volume":"119","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9257-0427","authenticated-orcid":false,"given":"Arkadeep","family":"Mitra","sequence":"first","affiliation":[{"name":"Genetics and Molecular Cardiology Laboratory, Department of Zoology University of Calcutta Kolkata West Bengal India"},{"name":"Department of Zoology City College 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