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. 2021 Jul 30;10(8):1939. doi: 10.3390/cells10081939

Figure 1.

Figure 1

Representative figure showing the general intracellular mechanisms of action of HSPs in heart and kidney. Normally in the cardiorenal axis HSPs 27, 60 and 70 are the ligands of TLR2 and TLR4 (more found in the hearts and kidneys), activating the p38 and IKK-NF-kB pathways. This pathway is responsible for inducing the expression of inflammatory and apoptosis genes (IL-1β, IL-6, IL-17, TNF-α and TGF-β). On the other side, the HSP90 is responsible for activating TGF-βR/SMAD2/3 pathway, responsible for inducing the expression of fibrotic genes (α-SMA and collagen). Physiological cell stress can also induce the production of endogenous HSPs. They are required to access to HSF1 complex present in the cytosol, allowing for its phosphorylation (P). The phosphorylated complex enters the nucleus and increases HSP expression in the cellular cytosol and outside. IL: interleukin; TLR: toll-like receptor, TNF-α: tumor necrosis factor alfa; TGF: transforming growth factor; TGFR: transforming growth factor receptor; HSF1: heat shock factor 1; SMA: smooth muscle actin.