has a pivotal function in various biological phenomena, including
neurogenesis, neuroregulation, chondrogenesis, cell growth, oncogenesis, immune balance and circandian
rhythm. Recently, DEC1 has received increasing attention for its role in maintaining the homeostasis
of metabolism and energy. Research has shown that DEC1 may play a vital role in metabolic disease.
Although the mechanism of the adverse reactions caused by quinolones has not been clarified, the distribution
of these serious adverse effects in tissues and organs is consistent with the expression of DEC1
in corresponding normal tissues. In the present paper, we review evidence showing that DEC1 may take
part in the adverse effects induced by quinolone antibiotics. The investigation of the molecular details
of the toxicity caused by quinolones may help overcome the shortcomings of the antibiotics and reveal
new, useful therapeutic functions besides their antimicrobial effect.