Post-transplant malignancy is one of the contentious and feared consequences of Solid Organ Transplantation (SOT), which might detrimentally alter the outcome of transplantation. Risk factors are manifold, principally related to a suppressed immune system with intercurrent immunosuppressant medications commonly used in the context of SOT. Opportunistic viral infections encountered in SOT are crucial promoters of mitogenic proliferation in several common tumors. Lastly, immune suppressant therapy might trigger mitogenic changes directly.In this paper, we are discussing post-SOT malignancies, elaborating on the different phases of its pathogenesis, and elucidating on the different aspects that linger in its risk factors, preventive strategies, and management.
Stroke is a clinically defined syndrome of acute focal neurological deficit attributed to vascular injury (infarction, hemorrhage) of the central nervous system. Stroke is the second leading cause of death and disability worldwide. Stroke is not a single disease but can be caused by a wide range of risk factors, disease processes and mechanisms. Approximately 15% of strokes worldwide are the result of intracerebral hemorrhage, which can be deep (basal ganglia, brainstem), cerebellar or lobar. A minority (about 20%) of intracerebral hemorrhages are caused by macrovascular lesions (vascular malformations, aneurysms, cavernomas), venous sinus thrombosis or rarer causes.
Mitochondria are essential intracellular organelles that significantly influence various cellular processes, including metabolism, stress response, and cell fate. Their precise regulation is crucial for maintaining both organelle and cellular homeostasis. Wound healing is a complex, multifactorial process that relies on the coordinated actions of multiple cell types and numerous cellular mechanisms. Dysregulation in this process can lead to chronic wounds, which pose substantial challenges for healthcare systems and present limited treatment options due to their intricate pathogenesis. Recent research has increasingly focused on the role of mitochondria in wound healing, revealing their involvement in critical processes such as metabolism, apoptosis, and redox signaling. Mitochondrial dynamics play a vital role in wound healing by adapting to cellular demands and environmental cues. Moreover, mitophagy, the selective degradation of damaged mitochondria, is crucial for maintaining mitochondrial integrity and function during the healing process. Mitochondria are not only pivotal in energy production but also in calcium homeostasis and the generation of mitochondrial reactive oxygen species, which are essential for signaling during wound repair. As wound healing progresses through distinct yet overlapping stages mitochondria facilitate the energy demands of repair and contribute to cytoskeletal remodeling necessary for wound closure. Understanding the multifaceted roles of mitochondria in wound healing could lead to novel therapeutic approaches for chronic wounds. Future research should prioritize investigating mitochondrial dynamics and functions in human tissues to develop targeted strategies for enhancing wound healing outcomes.
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