Heat shock proteins (HSP) are a shock induced family of proteins, whose most prominent members are a group
of molecules dedicated to maintaining the function of other proteins. Interestingly, after being exposed to heat shock
typical proinflammatory agonists modify the heat shock-induced transcriptional program and expression of HSP genes,
suggesting a complex reciprocal regulation between the inflammatory pathway and that of the heat shock response. The
specific task of Heat shock protein 70 (Hsp 70), the most widespread and highly conserved HSP, is to protect against
inflammation through multiple mechanisms. So, the expression of immune reactivity to Hsp70 in the kidney could be a
cause of hypertension. Hsp70 modulates inflammatory response, as well as down-regulates the nuclear factor kappa-lightchain-
enhancer of activated B cells. Also, a decreased expression of renal Hsp70 may contribute to activate the toll-like
receptor 4-initiating inflammatory signal pathway.
In addition, several studies have revealed that Hsp70 is involved in the regulation of Angiotensin II, a peptide with proinflammatory
activity. Increased inflammatory response is generated by nicotinamide adenine dinucleotide phosphate
oxidase, following activation by Angiotensin II. Interestingly, Hsp70 protects the renal epithelium by modulation of
nicotinamide adenine dinucleotide phosphate oxidase, a fundamental step in the pro-inflammatory mechanism.
This article aims to summarize our understanding about possible mechanisms improving the renal inflammatory process
linked to Hsp70 expression. Finally, from a therapeutic point of view, the notion of antiinflammatory tools regulating
Hsp70 could directly affect the inflammatory renal disease.