Coordinated action among various organelles maintains cellular functions. For instance, mitochondria and lysosomes are the main organelles contributing to cellular metabolism and provide energy for cardiomyocyte contraction. They also provide essential signalling platforms in the cell that regulate many key processes such as autophagy, apoptosis, oxidative stress, inflammation and cell death. Often, abnormalities in mitochondrial or lysosomal structures and functions bring about cardiovascular diseases (CVDs). Although the communication between mitochondria and lysosomes throughout the cardiovascular system is intensely studied, the regulatory mechanisms have not been completely understood. Thus, we summarize the most recent studies related to mitochondria and lysosomes' role in CVDs and their potential connections and communications under cardiac pathophysiological conditions. Further, we discuss limitations and future perspectives regarding diagnosis, therapeutic strategies and drug discovery in CVDs.

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Oligodendrocytes are a type of glial cells that ensheath multiple neuronal axons and form myelin. Under pathological conditions, such as multiple sclerosis (MS), inflammatory damage to myelin and oligodendrocytes leads to demyelination. Although the demyelinated regions can partially resolve functional deficits through remyelination, however, as the disease progresses, remyelination typically becomes incomplete and ultimately fails. One possible explanation for this failure is the activation of the Notch pathway in MS lesions, which impedes oligodendrocyte precursor cells (OPCs) at maturation. This leads to a potential target for remyelination. Here, we have identified a compound Yhhu4952 that promoted the maturation of cultured OPCs in a dose-dependent and time-dependent manner. Neonatal rats showed a significant increase in the expression of myelin basic protein (MBP) and the prevalence of mature oligodendrocytes in the corpus callosum after Yhhu4952 treatment. The compound was also effective in promoting remyelination in cuprizone-induced demyelination model and improving severity scores in experimental autoimmune encephalomyelitis (EAE) model. Mechanism studies revealed that Yhhu4952 promotes OPC differentiation through the inhibition of the Jagged1-Notch1 pathway. These findings suggest Yhhu4952 is potentially useful for proceeding oligodendrocyte differentiation and remyelination.