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Additionally, HIF-1α knock-out mice develop less clinical signs of sepsis [24].
Two other studies have documented that Tlr4-deficient mice develop less renal fibrosis after UUO [23], [34].
The reduced expression of IL-18 in epididymal WAT is of special interest, since ApoE−/− IL-18−/− mice develop less atherosclerosis than control ApoE−/− mice [21].
Taken together these results show that FcRγ−/− mice develop less IgG1 and C3c deposits in the splenic vessel walls and lower IgG1 titre in the renal mesangium compared to Hg-treated wt mice.
The role of IL-17 specifically in CAIA is fairly unstudied; however, IL-17 knockout mice develop less severe arthritis than wildtype controls in the K/BxN serum transfer arthritis model [ 18].
Interestingly, scid/mdx mice develop less fibrosis in the diaphragm at one year of age, which correlates with a decrease in TGF β protein in the dystrophic muscle [ 58].
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Similarly, properdin-deficient transgene Cfp-/ mice develop less-severe K/BxN arthritis [ 35].
Despite the lack of requirement for NOX2 for the development of pressure overload hypertrophy, it was found that NOX2 knockout mice developed less interstitial fibrosis and contractile dysfunction than wild-type littermates [ 41] indicating a dissociation between hypertrophy per se and fibrosis or contractile dysfunction.
Finally, after liver injury, GRK2-deficient mice developed less severe portal hypertension than control mice.
We recently described the accelerated induction of anti-DNA Abs in NZB/NZW mice immunized with Escherichia coli (EC) dsDNA; paradoxically these mice developed less renal disease than unimmunized mice or mice immunized with calf thymus DNA.
Mmp8−/− mice developed less fibrosis than their wildtype counterparts.
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