Altered responsiveness to extracellular ATP enhances acetaminophen hepatotoxicity

@inproceedings{Amaral2012AlteredRT,
  title={Altered responsiveness to extracellular ATP enhances acetaminophen hepatotoxicity},
  author={Sylvia Stella Amaral and Andr{\'e} Gustavo Fernandes Oliveira and Pedro Elias Marques and Jayane L D Quint{\~a}o and Daniele Ara{\'u}jo Pires and Rodrigo Ribeiro Resende and Bruna Ranyelle de Marinho Sousa and Juliana Gil Melgaço and Marcelo Pinto and Remo C Russo and Ariane K. C. Gomes and L{\'i}dia M Andrade and Rafael Fernandes Zanin and Rafaela Vaz Sousa Pereira and Cristina Bonorino and Frederico M. Soriani and Cristiano Xavier Lima and Denise Carmona Cara and Mauro M Teixeira and Maria de F{\'a}tima M. P. Leite and Gustavo Batista Menezes},
  booktitle={Cell Communication and Signaling},
  year={2012}
}
Adenosine triphosphate (ATP) is secreted from hepatocytes under physiological conditions and plays an important role in liver biology through the activation of P2 receptors. Conversely, higher extracellular ATP concentrations, as observed during necrosis, trigger inflammatory responses that contribute to the progression of liver injury. Impaired calcium (Ca2+) homeostasis is a hallmark of acetaminophen (APAP)-induced hepatotoxicity, and since ATP induces mobilization of the intracellular Ca2… CONTINUE READING
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