A promising therapeutic peptide and preventive/diagnostic biomarker for age-related diseases: The Elabela/Apela/Toddler peptide

Neuroinflammation and Neurodegenerative Diseases: How Much Do We Still Not Know?

“…Furthermore, ELA-32 administration has been revealed to ameliorate neuronal ferroptosis, iron deposition, mitochondrial damage, lipid peroxidation, and glutathione reduction. These results have emphasized the role of the ELA-APJ axis in attenuating neuronal ferroptosis after ischemic stroke (widely quoted in [13]). However, further data are needed to provide other/novel strategies to modulate the onset of neuroinflammation and ND, such as stroke.…”

“…However, the precise molecular mechanisms underlying the involvement of ferroptosis in the pathological processes of neurodegeneration and its impact on neuronal dysfunction remain to be discovered. Nevertheless, ferroptosis has recently been reported to likely be regulated by ELA/APJ signaling of the apelinergic system [13], where ELA is a peptide hormone belonging to the adipokine group and a component of the apelinergic system, discovered in 2013-2014 [13]. This relationship, mediated by ELA/APJ signaling, might be a promising strategy for the treatment of NDs, such as stroke [13].…”

“…Nevertheless, ferroptosis has recently been reported to likely be regulated by ELA/APJ signaling of the apelinergic system [13], where ELA is a peptide hormone belonging to the adipokine group and a component of the apelinergic system, discovered in 2013-2014 [13]. This relationship, mediated by ELA/APJ signaling, might be a promising strategy for the treatment of NDs, such as stroke [13]. Accordingly, a recent study in mouse models of middle cerebral artery occlusion (MCAO) has demonstrated the protective role of the ELA-APJ axis in ischemic stroke after treatment with ELA-32 (widely quoted in [13]).…”

“…This relationship, mediated by ELA/APJ signaling, might be a promising strategy for the treatment of NDs, such as stroke [13]. Accordingly, a recent study in mouse models of middle cerebral artery occlusion (MCAO) has demonstrated the protective role of the ELA-APJ axis in ischemic stroke after treatment with ELA-32 (widely quoted in [13]). A reduction in cerebral ischemic lesion and an improvement in neurobehavioral and cognitive deficits have been detected.…”

“…Such has led some to suppose that variations in the iron metabolism's homeostasis, the consequent induction of oxidative stress, and the related inflammation in the CNS is involved in the onset of ferroptosis and neuronal health [10][11][12]. In such a process, the apelinergic system, mediated by ELA/APJ signaling, has also been recently documented to participate in this regulation [13]. Another nonclassical mechanism related to onset of neuroinflammation appears to be the modified expression of neurotrophins, such as BDNF [14].…”