The renin-angiotensin-aldosterone system (RAAS) has a significant act in the pathology of blood pressure and cancer. One of the dominant sections of angiotensin II (Ang II) and angiotensin-converting enzyme (ACE) expression generation in the human body is the capillary veins in the lung. Changes in the expression of RAAS were revealed to be included in several lung diseases. There are several studies on the anticancer effect of ACE inhibitors; however, Hicks and colleagues reported an augmented risk of 14% for advancing lung cancer for patients consuming ACE inhibitors against angiotensin receptor blockers (ARBs) administration. Several lines of evidence indicated that ARB users have a lower risk of tumor progression and metastasis and progression of lung cancer. This review has surveyed some studies about the study by Hicks et al with conflicting results. Some Hicks’s study limitations are summarized here such as genetic effects, comparative study, residual confounding factors such as smoking, detection bias owing to cough, and socio-economic status. It is suggested some natural alternatives to ACE Inhibitors in here.
Renal fibrosis is the hallmark of advanced chronic kidney disease (CKD), which is characterized by excessive accumulation of extracellular matrix (ECM) proteins and plays a central role in the pathogenesis and progression of CKD to end-stage renal disease (ESRD). The molecular and cellular substances of kidney fibrosis include growth factors, such as fibroblast growth factor (FGF), transforming growth factor beta (TGF-β) and platelet-derived growth factor (PDGF), alongside cytokines (like interleukin-1b) and metalloproteinases. Therefore, these factors can be evaluated as possible targets for anti-fibrotic agents. Among the mediators of fibrosis, TGF-β is the dominant facilitator of renal fibrosis that induces ECM construction and accumulation. Numerous studies have focused on the inhibition of TGF-β and its downstream targets for the treatment of renal disease. Abolition of TGF-β mRNA expression was found to be the mechanism of anti-fibrotic drug, pirfenidone, in the heart and kidneys of diabetic rats. Various investigations have shown the impact of pirfenidone in diminishing kidney fibrosis, with studies containing patients diagnosed with subtotal nephrectomy, diabetic kidney disease and unilateral ureteral obstruction (UUO), administered drugs such as cyclosporine, tacrolimus, doxorubicin and vanadate. Several therapeutic drugs for fibrosis reduce only one of the oxidative, inflammatory or profibrogenic markers, while pirfenidone targets all three of these markers and therefore, seems to be a particularly valuable drug.
Curcumin is the essential ingredient of turmeric and one of the most potent antioxidants. It also has several biological capabilities, including anti-inflammatory, anticarcinogenic, anticoagulant, antidiabetic, antiviral, antibacterial, and antifungal effects. Therefore, curcumin has a significant potential for the treatment and control of various diseases. In kidney disorders like chronic kidney disease (CKD) and diabetic nephropathy (DN), the mechanism of kidney damage is associated with oxidative stress and inflammation. Curcumin, which has antioxidant and anti-inflammatory abilities, can alleviate kidney damage and treat kidney diseases. In patients with kidney disorders, progression to end-stage renal disease (ESRD) is critical because it increases their mortality rate. It has also been proved that curcumin could diminish such progression due to its antioxidant and anti-inflammatory potential, improving the survival rate. Besides, it has numerous nephroprotective effects that are summarized in this review.
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