![]() ![]() In microautophagy, the membrane of the lysosome invaginated and differentiates into an autophagic tube to enclose or engulf the cytosol directly. Following delivery to the vacuole or lysosome, the cargo is degraded and the resulting macromolecules are released back into the cytosol for reuse. ![]() During macroautophagy, a double-membrane sequestering compartment is formed as phagophore and matures into an autophagosome. The term macroautophagy refers primarily to common autophagy. In mammalian cells, there are three predominant subtypes of autophagy: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). In this review, we provide an overview of the associations between autophagy, ER stress, and the UPR, as well as their roles in disease pathology, especially in ICH, and we highlight potential treatment strategies. With the growing understanding of brain injury mechanisms after ICH, preventing brain injury and promoting neuronal survival have emerged as therapeutic goals. 20% of patients are functionally independent at 6 months after experiencing ICH, and survivors often suffer from serious neurologic impairments. As a subtype of stroke, intracerebral hemorrhage (ICH) is often associated with high mortality and morbidity, as well as with poor clinical outcomes. It has been widely reported that autophagy is associated with several neurologic diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), subarachnoid hemorrhage and ICH. The significant role of the ER stress-associated UPR in disease has been well studied. The eventual outcome of ER stress determines whether a cell survives or undergoes programmed cell death. As misfolded proteins accumulate, the unfolded protein response (UPR) is initiated to counter these stress effects. When a cell experiences stress conditions, such as starvation, redox imbalance, altered protein glycosylation, or protein folding defects, the normal functioning of the ER in protein synthesis is disrupted, and the ER switches to a stress state. The endoplasmic reticulum (ER) is an organelle wherein proteins are synthesized, matured, and secreted. ![]() This intracellular mechanism is essential for cell survival, facilitating the breakdown and eventual recycling of macromolecules during cellular adaptation to environmental changes. We also provide an overview of therapeutic approaches that target autophagy, and we discuss the prospects for modulating autophagy, ER stress, and UPR mechanisms in ICH therapy.Īutophagy plays an important role in cell metabolism and disease pathology. In this review, we summarize the related studies and highlight the roles of autophagy, ER stress, and the UPR in disease, especially in ICH. An understanding of the mechanisms of injury and recovery after ICH is crucial to develop therapeutic strategies. Whether these mechanisms are beneficial or detrimental remains a matter of controversy, but there is no doubt as to their vital functions. As an important mechanism of cell homeostasis, autophagy has been widely studied, and the associations between autophagy, ER stress, and the UPR have also been demonstrated. As a result of the injury, cell metabolism is disrupted and a series of stress responses are activated, such as endoplasmic reticulum (ER) stress and the unfolded protein response (UPR), leading to the re-establishment of cell homeostasis or cell death. Intracerebral hemorrhage (ICH) is a subtype of stroke that is followed by primary and secondary brain injury. ![]()
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