Evidences a(CHEBI:heme) to p(MGI:Hmox1)

The results showed that enforced HO-1 could efficiently decline the heme level in the lysates of ligated kidneys, and inhibit kidney inflammation characterized by down-regulation of NLRP3-Caspase- 1-IL-1b axis.

Heme induced the expression of Ho1 and Blvrb as well as Slc40a1, which encodes the mammalian iron exporter (Figure 5A), in agreement with previous reports (Delaby et al., 2008).

The Hmox1 (− /− ) MEF cells expressed no functional Hmox1 mRNA (Figure 1a) and as a result accumulated more cell-associated heme during extracellular exposure compared with wild-type cells (Figure 1b).

Exposure to Hb and its oxidized products increases heme overload on the AT1 cells. Heme overload induces the expression of HO-1 and iron-sequestering proteins, such as ferritin.

Mice lacking HO-1 (Hmox1−/−) are highly susceptible to pathologic conditions associated with increased serum heme concentration.

Macrophages are crucial for the removal of excess heme resulting from hemolysis via the uptake and degradation of heme by HO-1 (ref. 23), encoded by Hmox1.

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.