Metformin-mediated protection against doxorubicin-induced cardiotoxicity DOI Open Access
Ming‐Li Sun, Junfeng Dong, Chen Liu

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 180, P. 117535 - 117535

Published: Oct. 15, 2024

Language: Английский

The Dual Function of Autophagy in Doxorubicin-induced Cardiotoxicity: Mechanism and Natural products DOI
Nannan Tan, Hanwen Luo, Weili Li

et al.

Seminars in Cancer Biology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

1
The mechanism and therapeutic strategies in Doxorubicin induced cardiotoxicity: Role of programmed cell death DOI Creative Commons
Yanzhao Li, Jing Yan, Pingzhen Yang

et al.

Cell Stress and Chaperones, Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 1, 2024

Language: Английский

Citations

7
Enhanced SIRT3 expression restores mitochondrial quality control mechanism to reverse osteogenic impairment in type 2 diabetes mellitus DOI Creative Commons

Yansi Xian,

Bin Liu, Tao Shen

et al.

Bone Research, Journal Year: 2025, Volume and Issue: 13(1)

Published: March 3, 2025

Abstract Osteoporosis represents a prevalent and debilitating comorbidity in patients diagnosed with type 2 diabetes mellitus (T2DM), which is characterized by suppressed osteoblast function disrupted bone microarchitecture. In this study, we utilized male C57BL/6 J mice to investigate the role of SIRT3 T2DM. Decreased expression impaired mitochondrial quality control mechanism are observed both vitro vivo models Mechanistically, suppression results hyperacetylation FOXO3, hindering activation PINK1/PRKN mediated mitophagy pathway resulting accumulation dysfunctional mitochondria. Genetical overexpression or pharmacological restores deacetylation status thus facilitating ameliorating osteogenic impairment Collectively, our findings highlight fundamental regulatory control, crucial for maintaining homeostasis These insights not only enhance understanding molecular mechanisms underlying diabetic osteoporosis but also identify as promising therapeutic target osteoporosis.

Language: Английский

Citations

0
Pathophysiology of Doxorubicin-Mediated Cardiotoxicity DOI Creative Commons
Roberto Arrigoni, Emilio Jirillo, Carlo Caiati

et al.

Toxics, Journal Year: 2025, Volume and Issue: 13(4), P. 277 - 277

Published: April 5, 2025

Doxorubicin (DOX) is used for the treatment of various malignancies, including leukemias, lymphomas, sarcomas, and bladder, breast, gynecological cancers in adults, adolescents, children. However, DOX causes severe side effects patients, such as cardiotoxicity, which encompasses heart failure, arrhythmia, myocardial infarction. DOX-induced cardiotoxicity (DIC) based on combination nuclear-mediated cardiomyocyte death mitochondrial-mediated death. Oxidative stress, altered autophagy, inflammation, apoptosis/ferroptosis represent main pathogenetic mechanisms responsible DIC. In addition, vitro vivo models DIC sirtuins (SIRT), especially, SIRT 1 are reduced, this event contributes to cardiac damage. fact, inhibits reactive oxygen species NF-kB activation, thus improving oxidative stress remodeling. Therefore, recovery during may a therapeutic strategy limit progression. Natural products, i.e., polyphenols, well nano formulations iron chelators, other potential compounds experimented with At present, few clinical trials available confirm efficacy these products The aim review description pathophysiology drug targets alleviate

Language: Английский

Citations

0
Metformin-mediated protection against doxorubicin-induced cardiotoxicity DOI Open Access
Ming‐Li Sun, Junfeng Dong, Chen Liu

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 180, P. 117535 - 117535

Published: Oct. 15, 2024

Language: Английский

Citations

2