@misc{MTMT:33094535,
	title = {Egy ismert gyógyszermetabolit, a Desethylamiodarone potenciális szerepe az invazív hólyagdaganatok kezelésében},
	url = {https://m2.mtmt.hu/api/publication/33094535},
	author = {Bognár, Zita and Bognár, Rita and Ramadan, Fadi and Sümegi, Balázs},
	unique-id = {33094535},
	year = {2022}
}

@article{MTMT:31840534,
	title = {BGP-15 Protects against Heart Failure by Enhanced Mitochondrial Biogenesis and Decreased Fibrotic Remodelling in Spontaneously Hypertensive Rats},
	url = {https://m2.mtmt.hu/api/publication/31840534},
	author = {Horváth, Orsolya and Takács-Ördög, Katalin and Bruszt, Kitti and Deres, László and Gallyas, Ferenc and Sümegi, Balázs and Tóth, Kálmán and Halmosi, Róbert},
	doi = {10.1155/2021/1250858},
	journal-iso = {OXID MED CELL LONGEV},
	journal = {OXIDATIVE MEDICINE AND CELLULAR LONGEVITY},
	volume = {2021},
	unique-id = {31840534},
	issn = {1942-0900},
	year = {2021},
	eissn = {1942-0994},
	orcid-numbers = {Horváth, Orsolya/0000-0002-5456-7200; Takács-Ördög, Katalin/0000-0002-8269-7256; Bruszt, Kitti/0000-0002-7544-009X; Deres, László/0000-0003-1808-3724; Gallyas, Ferenc/0000-0002-1906-4333; Tóth, Kálmán/0000-0002-0114-5231; Halmosi, Róbert/0000-0002-6965-7743}
}

@article{MTMT:31822211,
	title = {Cyclophilin D-dependent mitochondrial permeability transition amplifies inflammatory reprogramming in endotoxemia},
	url = {https://m2.mtmt.hu/api/publication/31822211},
	author = {Veres, Balázs and Erős, Krisztián and Antus, Csenge Petra and Kálmán, Nikoletta and Fónai, Fruzsina and Jakus, Péter and Boros, Éva and Hegedűs, Zoltán and Nagy, István and Tretter, László and Gallyas, Ferenc and Sümegi, Balázs},
	doi = {10.1002/2211-5463.13091},
	journal-iso = {FEBS OPEN BIO},
	journal = {FEBS OPEN BIO},
	volume = {11},
	unique-id = {31822211},
	issn = {2211-5463},
	abstract = {Microorganisms or LPS (lipopolysaccharide), an outer membrane component of Gram-negative bacteria, can induce a systemic inflammatory response that leads to sepsis, multiple organ dysfunction, and mortality. Here, we investigated the role of cyclophilin D (CypD)-dependent mitochondrial permeability transition (mPT) in the immunosuppressive phase of LPS-induced endotoxic shock. The liver plays an important role in immunity and organ dysfunction; therefore, we used liver RNA sequencing (RNAseq) data, Ingenuity® Pathway Analysis (IPA ® ) to investigate the complex role of mPT formation in inflammatory reprogramming and disease progression. LPS induced significant changes in the expression of 2844 genes, affecting 179 pathways related to mitochondrial dysfunction, defective oxidative phosphorylation, nitric oxide (NO) and reactive oxygen species (ROS) accumulation, nuclear factor, erythroid 2 like 2 (Nrf2), Toll-like receptors (TLRs), and tumor necrosis factor α receptor (TNFR)-mediated processes in wild-type mice. The disruption of CypD reduced LPS-induced alterations in gene expression and pathways involving TNFRs and TLRs, in addition to improving survival and attenuating oxidative liver damage and the related NO- and ROS-producing pathways. CypD deficiency diminished the suppressive effect of LPS on mitochondrial function, nuclear- and mitochondrial-encoded genes, and mitochondrial DNA (mtDNA) quantity, which could be critical in improving survival. Our data propose that CypD-dependent mPT is an amplifier in inflammatory reprogramming and promotes disease progression. The mortality in human sepsis and shock is associated with mitochondrial dysfunction. Prevention of mPT by CypD disruption reduces inflammatory reprogramming, mitochondrial dysfunction, and lethality; therefore, CypD can be a novel drug target in endotoxic shock and related inflammatory diseases.},
	keywords = {Inflammation; LIVER; ENDOTOXIN; ANTIOXIDANT; Mitochondria; Gene Expression; Toll-like receptor; Reprogramming; cyclophilin D; Oxidative stress},
	year = {2021},
	eissn = {2211-5463},
	pages = {684-704},
	orcid-numbers = {Tretter, László/0000-0001-5638-2886; Gallyas, Ferenc/0000-0002-1906-4333}
}

@misc{MTMT:33094592,
	title = {Amiodarone’s major metabolite, desethylamiodarone inhibits proliferation and in vivo metastasizing property of B16-F10 melanoma cells},
	url = {https://m2.mtmt.hu/api/publication/33094592},
	author = {Bognár, Zita and Cseh, Anna Mária and Fekete, Katalin and Antus, Csenge Petra and Bognár, Rita and Tapodi, Antal and Ramadan, Fadi and Sümegi, Balázs and Gallyas, Ferenc},
	unique-id = {33094592},
	year = {2020},
	orcid-numbers = {Gallyas, Ferenc/0000-0002-1906-4333}
}

@article{MTMT:31659630,
	title = {Resveratrol Improves Heart Function by Moderating Inflammatory Processes in Patients with Systolic Heart Failure},
	url = {https://m2.mtmt.hu/api/publication/31659630},
	author = {Gál, Roland and Deres, László and Horváth, Orsolya and Erős, Krisztián and Sándor, Barbara and Urbán, Péter and Soós, Szilvia and Márton, Zsolt and Sümegi, Balázs and Tóth, Kálmán and Habon, Tamás and Halmosi, Róbert},
	doi = {10.3390/antiox9111108},
	journal-iso = {ANTIOXIDANTS-BASEL},
	journal = {ANTIOXIDANTS},
	volume = {9},
	unique-id = {31659630},
	year = {2020},
	eissn = {2076-3921},
	orcid-numbers = {Sándor, Barbara/0000-0002-7028-4227; Habon, Tamás/0000-0002-4816-857X}
}

@article{MTMT:31617910,
	title = {Amiodarone's major metabolite, desethylamiodarone inhibits proliferation of B16-F10 melanoma cells and limits lung metastasis formation in an in vivo experimental model},
	url = {https://m2.mtmt.hu/api/publication/31617910},
	author = {Bognár, Zita and Cseh, Anna Mária and Fekete, Katalin and Antus, Csenge Petra and Bognár, Rita and Tapodi, Antal and Ramadan, Fadi and Sümegi, Balázs and Gallyas, Ferenc},
	doi = {10.1371/journal.pone.0239088},
	journal-iso = {PLOS ONE},
	journal = {PLOS ONE},
	volume = {15},
	unique-id = {31617910},
	issn = {1932-6203},
	abstract = {Previously, we demonstrated the in vitro anti-tumor effects of desethylamiodarone (DEA) in bladder and cervix cancer cell lines. In the present study, we intended to establish its potentiality in B16-F10 metastatic melanoma cells in vitro and in vivo. We assessed cell proliferation, apoptosis and cell cycle by using sulforhodamine B assay, Muse™ Annexin V & Dead Cell and Muse® Cell Cycle assays, respectively. We determined colony formation after crystal violet staining. For studying mechanistic aspects, immunoblotting analysis was performed. We used a C57BL/6 experimental lung metastasis model for demonstrating in vivo anti-metastatic potential of DEA. DEA inhibited in vitro proliferation and colony formation, and in vivo lung metastasizing properties of B16-F10 cells. It arrested the cells in G0/G1 phase of their cycle likely via p21 in a p53-dependent fashion, and induced caspase mediated apoptosis likely via inversely regulating Bcl-2 and Bax levels, and reducing Akt and ERK1/2 activation. In this study, we provided in vitro and in vivo experimental evidences for DEA's potentiality in the therapy of metastatic melanomas. Since DEA is the major metabolite of amiodarone, a worldwide used antiarrhythmic drug, safety concerns could be resolved more easily for it than for a novel pharmacological agent.},
	year = {2020},
	eissn = {1932-6203},
	orcid-numbers = {Gallyas, Ferenc/0000-0002-1906-4333}
}

@article{MTMT:31288947,
	title = {Mitochondrial Protection by PARP Inhibition},
	url = {https://m2.mtmt.hu/api/publication/31288947},
	author = {Gallyas, Ferenc and Sümegi, Balázs},
	doi = {10.3390/ijms21082767},
	journal-iso = {INT J MOL SCI},
	journal = {INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES},
	volume = {21},
	unique-id = {31288947},
	issn = {1661-6596},
	abstract = {Inhibitors of the nuclear DNA damage sensor and signalling enzyme poly(ADP-ribose) polymerase (PARP) have recently been introduced in the therapy of cancers deficient in double-strand DNA break repair systems, and ongoing clinical trials aim to extend their use from other forms of cancer non-responsive to conventional treatments. Additionally, PARP inhibitors were suggested to be repurposed for oxidative stress-associated non-oncological diseases resulting in a devastating outcome, or requiring acute treatment. Their well-documented mitochondria- and cytoprotective effects form the basis of PARP inhibitors' therapeutic use for non-oncological diseases, yet can limit their efficacy in the treatment of cancers. A better understanding of the processes involved in their protective effects may improve the PARP inhibitors' therapeutic potential in the non-oncological indications. To this end, we endeavoured to summarise the basic features regarding mitochondrial structure and function, review the major PARP activation-induced cellular processes leading to mitochondrial damage, and discuss the role of PARP inhibition-mediated mitochondrial protection in several oxidative stress-associated diseases.},
	keywords = {APOPTOSIS; AKT; AIF; Cell Death; MAPK; ROS; MPT},
	year = {2020},
	eissn = {1422-0067},
	orcid-numbers = {Gallyas, Ferenc/0000-0002-1906-4333}
}

@article{MTMT:31202699,
	title = {Role of Akt Activation in PARP Inhibitor Resistance in Cancer},
	url = {https://m2.mtmt.hu/api/publication/31202699},
	author = {Gallyas, Ferenc and Sümegi, Balázs and Szabo, Csaba},
	doi = {10.3390/cancers12030532},
	journal-iso = {CANCERS},
	journal = {CANCERS},
	volume = {12},
	unique-id = {31202699},
	abstract = {Poly(ADP-ribose) polymerase (PARP) inhibitors have recently been introduced in the therapy of several types of cancers not responding to conventional treatments. However, de novo and acquired PARP inhibitor resistance is a significant limiting factor in the clinical therapy, and the underlying mechanisms are not fully understood. Activity of the cytoprotective phosphatidylinositol-3 kinase (PI3K)-Akt pathway is often increased in human cancer that could result from mutation, expressional change, or amplification of upstream growth-related factor signaling elements or elements of the Akt pathway itself. However, PARP-inhibitor-induced activation of the cytoprotective PI3K-Akt pathway is overlooked, although it likely contributes to the development of PARP inhibitor resistance. Here, we briefly summarize the biological role of the PI3K-Akt pathway. Next, we overview the significance of the PARP-Akt interplay in shock, inflammation, cardiac and cerebral reperfusion, and cancer. We also discuss a recently discovered molecular mechanism that explains how PARP inhibition induces Akt activation and may account for apoptosis resistance and mitochondrial protection in oxidative stress and in cancer.},
	keywords = {CYTOPROTECTION; mTor; PI3K; apoptosis resistance; PARP-Akt interplay; mitochondrial protection; Oxidative stress},
	year = {2020},
	eissn = {2072-6694},
	orcid-numbers = {Gallyas, Ferenc/0000-0002-1906-4333}
}

@article{MTMT:30900106,
	title = {BGP-15 Protects Mitochondria in Acute, Acetaminophen Overdose Induced Liver Injury},
	url = {https://m2.mtmt.hu/api/publication/30900106},
	author = {Sarnyai, Farkas and Szekerczés, Tímea and Csala, Miklós and Sümegi, Balázs and Szarka, András and Schaff, Zsuzsa and Mandl, József},
	doi = {10.1007/s12253-019-00721-1},
	journal-iso = {PATHOL ONCOL RES},
	journal = {PATHOLOGY AND ONCOLOGY RESEARCH},
	volume = {26},
	unique-id = {30900106},
	issn = {1219-4956},
	abstract = {Acetaminophen (APAP) induced hepatotoxicity involves activation of c-Jun amino-terminal kinase (JNK), mitochondrial damage and ER stress. BGP-15, a hydroximic acid derivative, has been reported to have hepatoprotective effects in APAP overdose induced liver damage. Effect of BGP-15 was further investigated on mitochondria in APAP-overdose induced acute liver injury in mice. We found that BGP-15 efficiently preserved mitochondrial morphology, and it caused a marked decrease in the number of damaged mitochondria. Attenuation of mitochondrial damage by BGP-15 is supported by immunohistochemistry as the TOMM20 label and the co-localized autophagy markers detected in the livers of APAP-treated mice were markedly reduced upon BGP-15 administration. This effect, along with the observed prevention of JNK activation likely contribute to the mitochondrial protective action of BGP-15.},
	keywords = {ACETAMINOPHEN; liver injury; BGP-15; reduced glutathione; Jun-kinase; Mitochondrium},
	year = {2020},
	eissn = {1532-2807},
	pages = {1797-1803},
	orcid-numbers = {Sarnyai, Farkas/0000-0002-5525-5508; Szekerczés, Tímea/0000-0002-7373-8730; Csala, Miklós/0000-0002-3829-4361; Szarka, András/0000-0001-6594-254X; Schaff, Zsuzsa/0000-0002-6429-8059; Mandl, József/0000-0001-9172-7202}
}

@article{MTMT:31279224,
	title = {Distribution and movement of water–soluble geochemical elements in a peat bog during environmental changes and human impacts in the Eastern Carpathians in Romania. Egy tőzegláp vízoldható geokémiai elemeinek eloszlása és mozgása a környezeti változások és emberi hatások tükrében, a Keleti-Kárpátokban},
	url = {https://m2.mtmt.hu/api/publication/31279224},
	author = {Tapody, Réka Orsolya and Törőcsik, Tünde and Fekete, István and Sümegi, Balázs and Sümegi, Pál},
	journal-iso = {ARCHEOMETRIAI MŰHELY},
	journal = {ARCHEOMETRIAI MŰHELY},
	volume = {16},
	unique-id = {31279224},
	issn = {1786-271X},
	year = {2019},
	pages = {205-213},
	orcid-numbers = {Sümegi, Pál/0000-0003-1755-4440}
}