Literature DB >> 31858156

The vital role of ATP citrate lyase in chronic diseases.

Amrita Devi Khwairakpam1, Kishore Banik1, Sosmitha Girisa1, Bano Shabnam1, Mehdi Shakibaei2, Lu Fan3, Frank Arfuso4, Javadi Monisha1, Hong Wang3, Xinliang Mao5,6, Gautam Sethi7, Ajaikumar B Kunnumakkara8.   

Abstract

Chronic or non-communicable diseases are the leading cause of death worldwide; they usually result in long-term illnesses and demand long-term care. Despite advances in molecular therapeutics, specific biomarkers and targets for the treatment of these diseases are required. The dysregulation of de novo lipogenesis has been found to play an essential role in cell metabolism and is associated with the development and progression of many chronic diseases; this confirms the link between obesity and various chronic diseases. The main enzyme in this pathway-ATP-citrate lyase (ACLY), a lipogenic enzyme-catalyzes the critical reaction linking cellular glucose catabolism and lipogenesis. Increasing lines of evidence suggest that the modulation of ACLY expression correlates with the development and progressions of various chronic diseases such as neurodegenerative diseases, cardiovascular diseases, diabetes, obesity, inflammation, and cancer. Recent studies suggest that the inhibition of ACLY activity modulates the glycolysis and lipogenesis processes and stimulates normal physiological functions. This comprehensive review aimed to critically evaluate the role of ACLY in the development and progression of different diseases and the effects of its downregulation in the prevention and treatment of these diseases.

Entities:  

Keywords:  ATP citrate lyase; Chronic diseases; Fatty acid biosynthesis; Lipogenic enzyme

Mesh:

Substances:

Year:  2019        PMID: 31858156     DOI: 10.1007/s00109-019-01863-0

Source DB:  PubMed          Journal:  J Mol Med (Berl)        ISSN: 0946-2716            Impact factor:   4.599


  262 in total

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6.  Enhanced glycerol 3-phosphate dehydrogenase activity in adipose tissue of obese humans.

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10.  IGF1-mediated HOXA13 overexpression promotes colorectal cancer metastasis through upregulating ACLY and IGF1R.

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