Cardiovascular Therapy Benefits of Novel Antidiabetic Drugs in Patients With Type 2 Diabetes Mellitus Complicated With Cardiovascular Disease: A Network Meta-Analysis.

Objective: Provide an evidence-based basis for the selection of cardiovascular benefit drugs in Type 2 diabetes mellitus (T2DM) patients with cardiovascular disease (CVD).

Methods: Conduct a comprehensive search of all relevant literature from PubMed, Embase, Web of Science, Cochrane Library, and Clinical Trials.gov from their establishment until December 13, 2023, and select randomized controlled trials (RCTs) that meet the pre-established inclusion and exclusion criteria.

Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy.

Doxorubicin (DOX) is a powerful and commonly used chemotherapeutic drug, used alone or in combination in a variety of cancers, while it has been found to cause serious cardiac side effects in clinical application. More and more researchers are trying to explore the molecular mechanisms of DOX-induced cardiomyopathy (DIC), in which oxidative stress and inflammation are considered to play a significant role. This review summarizes signaling pathways related to oxidative stress and inflammation in DIC and compounds that exert cardioprotective effects by acting on relevant signaling pathways, including the role of Nrf2/Keap1/ARE, Sirt1/p66Shc, Sirt1/PPAR/PGC-1α signaling pathways and NOS, NOX, Fe signaling in oxidative stress, as well as the role of NLRP3/caspase-1/GSDMD, HMGB1/TLR4/MAPKs/NF-κB, mTOR/TFEB/NF-κB pathways in DOX-induced inflammation.

Research progress of therapeutic drugs for doxorubicin-induced cardiomyopathy.

Doxorubicin (DOX), as a kind of chemotherapy agent with remarkable therapeutic effect, can be used to treat diverse malignant tumors clinically. Dose-dependent cardiotoxicity is the most serious adverse reaction after DOX treatment, which eventually leads to cardiomyopathy and greatly limits the clinical application of DOX. DOX-induced cardiomyopathy is not a result of a single mechanistic action, and multiple mechanisms have been discovered and demonstrated experimentally, such as oxidative stress, inflammation, mitochondrial damage, calcium homeostasis disorder, ferroptosis, autophagy and apoptosis.