SHRSP

AcronymDefinition
SHRSPSpontaneously Hypertensive Rats-Stroke Prone (vascular research)
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Interesting observations were also reported with regard to Stim1 gene and the response to stress in SHRSP [34].
In the present paper, we will discuss the available evidence related to genes encoding mitochondrial proteins, underlying both stroke and renal damage development in SHRSP, that were discovered within STR1.
In the Search for Stroke Genes Mapping within the Stroke QTL STR1 in SHRSP
In fact, congenic lines were prepared by performing several backcrosses of SHRSP with SHRSR [8].
In particular, the mitochondrial dysfunction was discovered as a crucial mechanism underlying stroke development in SHRSP.
Notably, excess salt, through ROS produced by angiotensin II-activated NADPH oxidase, caused cerebral neuronal apoptosis and inflammation as well as stroke in SHRSP [49].
The SHRSP provides key insights into the contribution of mitochondrial dysfunction in the pathogenesis of vascular damage associated with hypertension.
Of note, treatment with S 35171, a compound able to protect mitochondrial function by increasing the inner antioxidant systems, was shown to delay and even to prevent brain damage in high salt fed SHRSP, as a result of protection from systemic processes linked to mitochondria and involved in brain damage [62].
Moreover, the significant protective effect described with fenofibrate on both renal and cerebral damage in salt loaded SHRSP [65] maybe mediated by its PPAR[alpha] agonist action and the consequent stimulation of UCP2 expression levels [66].
Through a microarray differential expression analysis, including all sequences mapping inside STR1, we discovered the gene encoding the mitochondrial protein Ndufc2 (a subunit of the OXPHOS complex I, encoded by nuclear DNA) as a sequence significantly downregulated by high salt diet only in the brain of SHRSP as compared to the SHRSR [13].
The observations obtained in the SHRSP reveal a key role of Ndufc2 in complex I assembly, a critical step for an appropriate complex I activity and for the whole OXPHOS function (Figure 1).
Whereas the above-mentioned evidence highlights the role of NDUFC2 as a novel gene for human diseases, the results obtained in SHRSP bring up to our attention for the first time the importance of an adequate mitochondrial function, through a regular complex I assembly and activity, in order to maintain the vascular health status and to avoid TOD development in hypertension.