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Vitamin D deficiency has been linked to several major chronic diseases, such as cardiovascular and neurodegenerative diseases, diabetes, and cancer, linked to oxidative stress, inflammation, and aging. Vitamin D deficiency appears to be particularly harmful to the cardiovascular system, as it can cause endothelial dysfunctioning and vascular abnormalities through the modulation of various downstream mechanisms. As a result, new research indicates that therapeutic approaches targeting vitamin D inadequacies or its significant downstream effects, such as impaired autophagy, abnormal pro-inflammatory and pro-oxidant reactions, may delay the onset and severity of major cerebrovascular disorders such as stroke and neurologic malformations. Vitamin D modulates the various molecular pathways, i.e., Nitric Oxide, PI3K-Akt Pathway, cAMP pathway, NF-kB Pathway, Sirtuin 1, Nrf2, FOXO, in cerebrovascular disorder. The current review shows evidence for vitamin D's mitigating or slowing the progression of these cerebrovascular disorders, which are significant causes of disability and death worldwide. [ABSTRACT FROM AUTHOR]

[Display omitted] • Oxidative stress and inflammation are two key contributors to neurodegenerative diseases (NDD). • Calcium and magnesium permeable ion channels are extensively expressed in neurones, hence TRPM 7 may prevent NDD. • TRPM7 control neuronal processes like cell survival, differentiation, migration, & synaptic transmission. • The activation of TRPM7 by PI3K, JAK-STAT, and MAPK can start a chain reaction of NDD activities. • TRPM7 dysregulation has been linked to numerous diseases including cancer, cardiovascular disease, and NDDs. The ions Ca2+ and Mg2+, which are both present in the body, have been demonstrated to be crucial in the control of a variety of neuronal processes. Transient melastatin-7 (TRPM7) channel plays an important role in controlling Ca2+ and Mg2+ homeostasis, which is crucial for biological processes. The review will also examine how changes in TRPM7 function or expression can lead to neurodegeneration. Even though eight different TRPM channels have been found so far, the channel properties, activation mechanisms, and physiological responses exhibited by these channels can vary greatly from one another. Only TRPM6 and TRPM7 out of the eight TRPM channels were found to have a high permeability to both Ca2+ and Mg2+. In contrast to TRPM6 channels, which are not highly expressed in neuronal cells, TRPM7 channels are widely distributed throughout the nervous system, so they will be the sole focus of this article. It is possible that, in the future, for the treatment of neurodegenerative disorder new therapeutic drug targets will be developed as a direct result of research into the specific roles played by TRPM7 channels in several different neurodegenerative conditions as well as the factors that are responsible for TRPM7 channel regulation. [ABSTRACT FROM AUTHOR]

Ischemic damage to the brain is linked to an increased rate of morbidity and mortality worldwide. In certain parts of the world, it remains a leading cause of mortality and the primary cause of long-term impairment. Ischemic injury is exacerbated when particular neuropeptides are removed, or their function in the brain is blocked, whereas supplying such neuropeptides lowers ischemic harm. Here, we have discussed the role of neuropeptides in ischemic injury. Numerous neuropeptides had their overexpression following cerebral ischemia. Neuropeptides such as NPY, CGRP, CART, SP, BK, PACAP, oxytocin, nociception, neurotensin and opioid peptides act as transmitters, documented in several "in vivo" and "in vitro" studies. Neuropeptides provide neuroprotection by activating the survival pathways or inhibiting the death pathways, i.e., MAPK, BDNF, Nitric Oxide, PI3k/Akt and NF-κB. Neuropeptides have numerous beneficial effects in ischemic models, including antiapoptotic, anti-inflammatory, and antioxidant actions that provide a powerful protective impact in neurons when combined. These innovative therapeutic substances have the potential to treat ischemia injury due to their pleiotropic modes of action. This review emphasizes the neuroprotective role of neuropeptides in ischemic injury via modulation of various signalling pathways i.e., MAPK, BDNF, Nitric Oxide, PI3k/Akt and NF-κB. [Display omitted] • Neuropeptides are critical for controlling the brain's response to various inputs and conditions, including ischemia • Neuropeptides are an element of the natural defense system in ischemic injury • Neuropeptides act as a neuroprotective agents in ischemic injury. • Neuropeptides play a critical part in the brain's self-preservation and recovery following ischemia • Neuropeptides such as PACAP, CGRP, and NPY show their neuroprotective effects by reducing apoptosis [ABSTRACT FROM AUTHOR]