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This regulation is altered in aged kidneys.
Therefore mitochondrial damage in aged kidneys seems to be associated with SIRT1 deficiency.
In aged kidneys, Picrosirius Red positive staining was increased in the interstitium (i.e. between tubules), and periglomerular areas.
Noteworthy was the close correlation in aged kidneys between the lower pericyte number and the following two changes in underlying peritubular microvessels.
Pericyte number associated with medullary peritubular capillaries was greatly reduced in aged kidneys (37.48 ± 2.14 vs. 20.74 ± 2.83, p < 0.006 vs. young adult).
In pre-capillary arterioles, pericyte number also decreased in aged kidneys (10.05±0.73 vs. 16.66±1.856 per field of view, p < 0.0062 vs. young adult mice).
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Data show that in aged kidney tissue, ferulate exhibited its antioxidative action by maintaining redox regulation, suppressing NF-κB activation and modulating the expression of NF-κB-induced, proinflammatory COX-2, iNOS, VCAM-1 and ICAM-1.
Adult-onset and long-term calorie restriction in mice increased Sirt1 expression in aged kidney and attenuated hypoxia-associated mitochondrial and renal damage by enhancing Bcl2/adenovirus E1B 19-kDa interacting protein 3- (Bnip3-) dependent autophagy.
There is a reduction in renal blood flow in aging, and aged kidneys have enhanced response to vasoconstrictors, and diminished response to vasodilators such as nitric oxide (reviewed in: [ 10].
A study of perivascular immune cell clusters and tertiary lymphoid organs (TLOs) in the aged kidneys of the same group of inbred strains as in the previous study identified associations with loci on Chr 1, Chr 2, Chr 8 and Chr 14 in male mice, which included the candidate genes Esrrg and Wisp2 (Huang et al., 2014).
In hypoxic aged kidneys, BNIP3 activation by caloric restriction promotes mitochondrial autophagy and thus enhances kidney adaptation to hypoxia [ 50].
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