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In hyperhomocysteinemia-induced myocardial injury, HS mitigates pathological progression through a four-pronged mechanism: (1) restoring CSE activity to lower plasma homocysteine levels, (2) reducing oxidative stress by decreasing lipid peroxidation product levels, (3) enhancing ROS scavenging through restored mitochondrial respiratory enzyme activity, and (4) inhibiting expression of ER stress markers (Chang et al., 2008)

Circumscribed glomeruli with normal architecture of capillary tufts was also noticed (Fig