The role of neurotrophins in psychopathology and cardiovascular diseases: psychosomatic connections.

Cardiovascular (CV) diseases and mood disorders are common public health problems worldwide. Their connections are widely studied, and the role of neurotrophins (NTs) is already supposed in both conditions. However, data in the literature of clinical aspects are sometimes controversial and no reviews are available describing possible associations between CV risk and mood disorders based on NTs. The mostly studied NT is brain-derived neurotrophic factor (BDNF). Decreased level of BDNF is observed in depression and its connection to hypertension has also been demonstrated with affecting the arterial baroreceptors, renin-angiotensin system and endothelial nitric oxide synthase. BDNF was also found to be the predictor of CV outcome in different patient populations. Other types of human NT-s, such as nerve growth factor, neurotrophin 3 and neurotrophin 4 also seem to have both psychopathological and CV connections. Our aim was to overview the present knowledge in this area, demonstrating a new aspect of the associations between mood disorders and CV diseases through the mediation of NTs. These findings might enlighten new psychosomatic connections and suggest new therapeutic targets that are beneficial both in respect of mood disorders and CV pathology.

The role of Sigma-1 receptor in sex-specific heat shock response in an experimental rat model of renal ischaemia/reperfusion injury.

We previously showed that female rats are more protected against renal ischaemia/reperfusion (I/R) injury than males, which is partly attributed to their more pronounced heat shock response. We recently described that Sigma-1 receptor (S1R) activation improves postischaemic survival and renal function. 17ß-estradiol activates S1R, thus here we investigated the role of sex-specific S1R activation and heat shock response in severe renal I/R injury. Proximal tubular cells were treated with 17ß-estradiol, which caused direct S1R activation and subsequent induction of heat shock response. Uninephrectomized female, male and ovariectomized female (Ovx) Wistar rats were subjected to 50-min renal ischaemia followed by 2 (T2) and 24 (T24) hours of reperfusion. At T24 renal functional, impairment was less severe and structural damage was less prominent in females versus males or Ovx. Postischaemic increase in S1R, pAkt, HSF-1, HSP72 levels were detected as early as at T2, while pHSP27 was elevated later at T24. Abundance of heat shock proteins was higher in healthy female rats and remained higher at T2 and T24 (female versus male or Ovx; resp.). We propose a S1R-dependent mechanism, which contributes to the relative renoprotection of females after I/R injury by enhancing the heat shock response.