Molecular Mechanism by Which TRPC6 Regulates Calcium Signaling and Neuroinflammation in the Onset and Development of Ischemic Stroke: A Review.

Abstract

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.