Altern Ther Health Med. 2024 Aug;30(8):170-175.
Cerebral infarction, also known as ischemic stroke, is caused by various regional blood supply disorders in the brain tissue, leading to ischemic hypoxic lesions and necrosis of the brain tissue and then the corresponding clinical manifestations of neurological loss, which has high mortality and disability. This study comprehensively reviews the potential molecular mechanisms of TRPC6 in neuroprotection in cerebral infarction and provides a summary of TRPC6 as a targeted drug or prognostic biomarker for cerebral infarction patients. We will screen and synthesize evidence about the molecular mechanisms of TRPC6 in cerebral infarction from the current literature to obtain comprehensive knowledge on this topic. In the pathogenesis, neuroinflammation and intracellular calcium accumulation play an important role in the onset and development of cerebral infarction. Transient receptor potential cation channel subfamily C6 (TRPC6) is the main component of calcium store-operated calcium channels. It plays a central role in ischemic cerebrovascular disease by mediating the calcium ion signaling pathway. In this review, evidence on the neuroprotective effects of TRPC6 has been shown, including inhibiting neuroinflammation and inhibiting nerve cell apoptosis, thereby alleviating nerve injury. However, at the same time, TRPC6 promotes inflammation in other organs. Generally, although an increasing number of researches support the protective role of TRPC6 in cerebral infarction, there is still evidence showing that overexpression of TRPC6 increases inflammatory tissue damage in other organs. Therefore, clarifying the molecular mechanism of TRPC6 will help develop targeted drugs or prognostic biomarkers for cerebral infarction to promote and predict neurological function recovery. More evidence to elucidate the molecular mechanism of TRPC6 in cerebral infarction is needed. Enriching TRPC6 in neuroinflammation areas and modifying its cell specificity might be the orientation of drug development that increases the effect of stroke treatment and reduces the impact on other organs. In conclusion, in cerebral infarction, TRPC6 has been proven to alleviate neuroinflammation and inhibit nerve cell apoptosis. However, at the same time, TRPC6 may promote inflammation in other organs. Therefore, the targeting potential of TRPC6 in cerebral infarction needs to be further explored.
脑梗死，又称缺血性脑卒中，是由于脑组织的各种区域性血液供应障碍引起的，导致脑组织的缺血缺氧性病变和坏死，进而出现相应的神经功能丧失的临床表现，具有较高的死亡率和致残率。本研究全面综述了 TRPC6 在脑梗死神经保护中的潜在分子机制，并总结了 TRPC6 作为脑梗死患者的靶向药物或预后生物标志物的研究进展。我们将从现有文献中筛选和综合有关 TRPC6 在脑梗死中的分子机制的证据，以获取该主题的综合知识。在发病机制中，神经炎症和细胞内钙积累在脑梗死的发生和发展中起重要作用。瞬时受体电位阳离子通道亚家族 C6（TRPC6）是钙库操纵钙通道的主要组成部分。它通过介导钙离子信号通路，在缺血性脑血管病中发挥核心作用。在本综述中，已经证明了 TRPC6 的神经保护作用的证据，包括抑制神经炎症和抑制神经细胞凋亡，从而减轻神经损伤。然而，与此同时，TRPC6 也会促进其他器官的炎症。一般来说，尽管越来越多的研究支持 TRPC6 在脑梗死中的保护作用，但仍有证据表明，TRPC6 的过表达会增加其他器官的炎症组织损伤。因此，阐明 TRPC6 的分子机制将有助于开发针对脑梗死的靶向药物或预后生物标志物，以促进和预测神经功能的恢复。需要更多的证据来阐明 TRPC6 在脑梗死中的分子机制。在神经炎症区域富集 TRPC6 并修饰其细胞特异性可能是药物开发的方向，这可以增加中风治疗的效果，减少对其他器官的影响。综上所述，在脑梗死中，TRPC6 已被证明可减轻神经炎症并抑制神经细胞凋亡。然而，与此同时，TRPC6 可能会促进其他器官的炎症。因此，TRPC6 在脑梗死中的靶向潜力需要进一步探索。
