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As a consequence of AKI, a significant number of oxygen free radicals are produced, endogenous antioxidants are continually depleted, and high levels of inflammatory substances are secreted, all of which contribute to kidney damage progression ( According to our published papers ( Our previously single-center clinical studies indicated CHF might have nephroprotection in A on C patients ( Ligusticum wallichii (Chuanxiong) , has the potential to prevent AKI via a variety of processes, including ameliorating oxidative stress damage, suppressing inflammatory responses, deterring apoptotic cell death of intrinsic renal cells, and modulating autophagy ( Renal fibrosis is by far the most important mechanism that leads to CKD ( 1 is the primary profibrotic facilitator in kidney disorders due to its role as a key modulator of fibrosis ( 1 have additionally validated the profibrotic function of TGF- 1 in the etiology of progressive renal fibrosis in a variety of kidney illnesses ( 1 might be a possible treatment target for the clinical management of renal fibrosis

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doi: 10.1371/journal.pone.0153677

In line with our hypothesis, raltitrexed also significantly increased mitochondrial content (Fig

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Canela VH, Bowen WS, Ferreira RM, Syed F, Lingeman JE, Sabo AR, et al