PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
35204799-0	2022	RRM2 Alleviates Doxorubicin-Induced Cardiotoxicity through the AKT/mTOR Signaling Pathway.	Doxorubicin	16-27	ribonucleotide reductase M2	Mus musculus	0-4	
35204799-4	2022	However, the specific function of RRM2 in DOX-induced cardiotoxicity is yet to be determined.	Doxorubicin	42-45	ribonucleotide reductase M2	Mus musculus	34-38	
35204799-5	2022	This study aimed to elucidate the role and potential mechanism of RRM2 on DOX-induced cardiotoxicity by investigating neonatal primary cardiomyocytes and mice treated with DOX.	Doxorubicin	74-77	ribonucleotide reductase M2	Mus musculus	66-70	
35204799-9	2022	RRM2 overexpression, on the contrary, alleviated DOX-induced cardiotoxicity in vivo and in vitro.	Doxorubicin	49-52	ribonucleotide reductase M2	Mus musculus	0-4	
35204799-11	2022	Mechanistically, we found that AKT/mTOR inhibitors could reverse the function of RRM2 overexpression on DOX-induced autophagy and apoptosis, which means that RRM2 could have regulated DOX-induced cardiotoxicity through the AKT/mTOR signaling pathway.	Doxorubicin	104-107	ribonucleotide reductase M2	Mus musculus	81-85	
35204799-11	2022	Mechanistically, we found that AKT/mTOR inhibitors could reverse the function of RRM2 overexpression on DOX-induced autophagy and apoptosis, which means that RRM2 could have regulated DOX-induced cardiotoxicity through the AKT/mTOR signaling pathway.	Doxorubicin	104-107	ribonucleotide reductase M2	Mus musculus	158-162	
35204799-11	2022	Mechanistically, we found that AKT/mTOR inhibitors could reverse the function of RRM2 overexpression on DOX-induced autophagy and apoptosis, which means that RRM2 could have regulated DOX-induced cardiotoxicity through the AKT/mTOR signaling pathway.	Doxorubicin	184-187	ribonucleotide reductase M2	Mus musculus	81-85	
35204799-11	2022	Mechanistically, we found that AKT/mTOR inhibitors could reverse the function of RRM2 overexpression on DOX-induced autophagy and apoptosis, which means that RRM2 could have regulated DOX-induced cardiotoxicity through the AKT/mTOR signaling pathway.	Doxorubicin	184-187	ribonucleotide reductase M2	Mus musculus	158-162	
35204799-12	2022	In conclusion, our experiment established that RRM2 could be a potential treatment in reversing DOX-induced cardiac dysfunction.	Doxorubicin	96-99	ribonucleotide reductase M2	Mus musculus	47-51