Mitochondrial quality control mechanisms as therapeutic targets in doxorubicin-induced cardiotoxicity

Trends in Pharmacological Sciences, Год журнала: 2022, Номер 44(1), С. 34 - 49

Опубликована: Ноя. 14, 2022

Язык: Английский

---

The role of autophagy in death of cardiomyocytes

Journal of Molecular and Cellular Cardiology, Год журнала: 2021, Номер 165, С. 1 - 8

Опубликована: Дек. 14, 2021

Autophagy mediates cellular quality control mechanisms and energy homeostasis through lysosomal degradation. is typically viewed as an adaptive process that allows cells to survive against stress, such nutrient deprivation hypoxia. However, autophagy also cell death during development in response stress. Cell accompanied by activation accumulation of autophagosomes has been classified type II programmed death. Compared the wealth knowledge regarding role autophagy, however, molecular which induces its functional significance are poorly understood. activated excessively under some conditions, causing uncontrolled degradation materials An imbalance between autophagosome formation causes a massive autophagosomes, subsequently dysfunction Dysregulation unique form death, termed autosis, with defined morphological biochemical features distinct from other forms apoptosis necrosis. In heart, dysregulated cardiomyocytes actively cardiac injury including reperfusion injury, doxorubicin cardiomyopathy, storage disorders. The goal this review introduce concept autophagic discuss various conditions.

Язык: Английский

---

Elabela ameliorates doxorubicin-induced cardiotoxicity by promoting autophagic flux through TFEB pathway

Pharmacological Research, Год журнала: 2022, Номер 178, С. 106186 - 106186

Опубликована: Март 17, 2022

Язык: Английский

---

Chemotherapy-induced cardiotoxicity: a new perspective on the role of Digoxin, ATG7 activators, Resveratrol, and herbal drugs

Journal of Medicine and Life, Год журнала: 2023, Номер 16(4), С. 491 - 500

Опубликована: Апрель 1, 2023

Cancer is a major public health problem, and chemotherapy plays significant role in the management of neoplastic diseases.However, chemotherapy-induced cardiotoxicity serious side effect secondary to cardiac damage caused by antineoplastic's direct indirect toxicity.Currently, there are no reliable approved methods for preventing or treating cardiotoxicity.Understanding mechanisms may be vital improving survival.The independent risk factors developing must considered prevent myocardial without decreasing therapeutic efficacy cancer treatment.This systematic review aimed identify analyze evidence on cardiotoxicity, associated factors, decrease it.We conducted comprehensive search PubMed, Google Scholar, Directory Open Access Journals (DOAJ) using following keywords: "doxorubicin cardiotoxicity", "anthracycline "chemotherapy", "digoxin "ATG7 activators", retrieving 59 articles fulfilling inclusion criteria.Therapeutic schemes can changed choosing prolonged infusion application over boluses.In addition, some agents like Dexrazoxane reduce high-risk groups.Recent research found that Digoxin, ATG7 activators, Resveratrol, other medical substances herbal compounds have comparable anthracycline-induced cardiotoxicity.

Язык: Английский

---

The transcriptional repressor HEY2 regulates mitochondrial oxidative respiration to maintain cardiac homeostasis

Nature Communications, Год журнала: 2025, Номер 16(1)

Опубликована: Янв. 2, 2025

Energy deprivation and metabolic rewiring of cardiomyocytes are widely recognized hallmarks heart failure. Here, we report that HEY2 (a Hairy/Enhancer-of-split-related transcriptional repressor) is upregulated in hearts patients with dilated cardiomyopathy. Induced Hey2 expression zebrafish or mammalian impairs mitochondrial respiration, accompanied by elevated ROS, resulting cardiomyocyte apoptosis Conversely, depletion adult mouse enhances the oxidation genes cardiac function. Multifaceted genome-wide analyses reveal enriches at promoters known to regulate metabolism (including Ppargc1, Esrra Cpt1) colocalizes HDAC1 effectuate histone deacetylation repression. Consequently, restoration PPARGC1A/ESRRA Hey2- overexpressing human cardiomyocyte-like cells rescues deficits bioenergetics. Knockdown protects against doxorubicin-induced dysfunction. These studies an evolutionarily conserved HEY2/HDAC1-Ppargc1/Cpt module controls energy preserve Mitochondrial dysfunction contributes pathogenesis during Here authors repressor regulates function hearts.

Язык: Английский

---

The Dual Function of Autophagy in Doxorubicin-induced Cardiotoxicity: Mechanism and Natural products

Seminars in Cancer Biology, Год журнала: 2025, Номер unknown

Опубликована: Янв. 1, 2025

Язык: Английский

---

Gasdermin D mediates endoplasmic reticulum stress via FAM134B to regulate cardiomyocyte autophagy and apoptosis in doxorubicin-induced cardiotoxicity

Cell Death and Disease, Год журнала: 2022, Номер 13(10)

Опубликована: Окт. 26, 2022

Abstract Cardiomyocyte pyroptosis and apoptosis play a vital role in the pathophysiology of several cardiovascular diseases. Our recent study revealed that gasdermin D (GSDMD) can promote myocardial I/R injury via caspase-11/GSDMD pathway. We also found GSDMD deletion attenuated MI by reducing cardiomyocyte pyroptosis. However, how mediates protects function remains unclear. Here, we doxorubicin (DOX) treatment resulted increased cardiomyocytes could mediate DOX-induced cardiotoxicity (DIC) injury. Interestingly, overexpression promoted apoptosis, which was knockdown. Notably, exacerbated DIC injury, impaired cardiac vitro vivo, enhanced autophagy. Mechanistically, regulated activity FAM134B, an endoplasmic reticulum autophagy receptor, pore formation on membrane its N-terminus, thus activating stress. In turn, FAM134B interacted with autophagic protein LC3, inducing autophagy, promoting aggravating DIC. These results suggest promotes induces modulating reaction thereby Targeted regulation may be new target for prevention

Язык: Английский

---

Cardiotoxicity of Anticancer Drugs: Molecular Mechanisms, Clinical Management and Innovative Treatment

Drug Design Development and Therapy, Год журнала: 2024, Номер Volume 18, С. 4089 - 4116

Опубликована: Сен. 1, 2024

With the continuous refinement of therapeutic measures, survival rate tumor patients has been improving year by year, while cardiovascular complications related to cancer therapy have become increasingly prominent. Exploring mechanism and prevention strategy therapy-related toxicity (CTR-CVT) remains one research hotspots in field Cardio-Oncology recent years. Cardiotoxicity anticancer drugs involves heart failure, myocarditis, hypertension, arrhythmias vascular toxicity, mechanistically endothelial dysfunction, ferroptosis, mitochondrial dysfunction oxidative stress. To address cardiotoxicity induced different drugs, various measures put place, such as reducing accumulation shifting with less cardiotoxicity, using cardioprotective early detection. Due very limited treatments available ameliorate drugs-induced a few innovations are being shifted from animal studies human studies. Examples include transplantation. Mitochondrial transplantation proven be effective vivo vitro experiments. Several demonstrated that intercellular transfer can doxorubicin(DOX)-induced laying foundation for innovative therapies cardiotoxicity. In this review, we will discuss current status terms pathogenesis treatment, focus on transplantation, hope review bring some inspiration you.

Язык: Английский

---

Aucubin alleviates doxorubicin-induced cardiotoxicity through crosstalk between NRF2 and HIPK2 mediating autophagy and apoptosis

Phytomedicine, Год журнала: 2024, Номер 127, С. 155473 - 155473

Опубликована: Фев. 21, 2024

Язык: Английский

---

The mechanism and therapeutic strategies in Doxorubicin induced cardiotoxicity: Role of programmed cell death

Cell Stress and Chaperones, Год журнала: 2024, Номер unknown

Опубликована: Сен. 1, 2024

Язык: Английский

---