Bartonellosis is an infectious disease caused by Bartonella species that are distributed worldwide with animal and public health impact varying according to Bartonella species, infection phase, immunological characteristics, and geographical region. Bartonella is widely present in various mammals including cats, rodents, ruminants, and humans. At least 13 Bartonella species or subspecies are zoonotic. Each species has few reservoir animals in which it is often asymptomatic. Bartonella infection may lead to various clinical symptoms in humans. As described in the B.tribocorum-rat model, when Bartonella was seeded into the blood stream, they could escape immunity, adhered to and invaded host erythrocytes. They then replicated and persisted in the infected erythrocytes for several weeks. This review summarizes the current knowledge of how Bartonella prevent phagocytosis and complement activation, what pathogenesis factors are involved in erythrocyte adhesion and invasion, and how Bartonella could replicate and persist in mammalian erythrocytes. Current advances in research will help us to decipher molecular mechanisms of interactions between Bartonella and mammalian erythrocytes and may help in the development of biological strategies for the prevention and control of bartonellosis.

Doxorubicin (Dox) is a chemotherapeutic agent widely used for the treatment of numerous cancers. However, the clinical use of Dox is limited by its unwanted cardiotoxicity. Mitochondrial dysfunction has been associated with Dox-induced cardiotoxicity. To mitigate Dox-related cardiotoxicity, considerable successful examples of a variety of small molecules that target mitochondria to modulate Dox-induced cardiotoxicity have appeared in recent years. Here, we review the related literatures and discuss the evidence showing that mitochondria-targeting small molecules are promising cardioprotective agents against Dox-induced cardiac events.