SLCO4C1 is the first member of the OATP family found to be predominantly expressed in the kidney. SLCO4C1, which is localized in the basolateral membrane of the proximal tubule, plays a major role in the urinary secretion of cardiac glycosides (digoxin and ouabain), thyroid hormones, cAMP, methotrexate, sitagliptin, estrone 3-sulfate, chenodeoxy cholic acid, and glycocholic acid. The OATP family includes sodium-independent organic anion transporters found in various tissues, including liver, kidney, intestine, and brain. OATP transporters facilitate transmembrane transport of bile acids, thyroid hormones, steroid conjugates, anionic oligopeptides, eicosanoids, various drugs, and other xenobiotic compounds. In humans, SLCO4C1 is the only organic anion transporter in the kidney, however, in rodent kidneys, several OATPs are present on the proximal basolateral and apical membranes.
|Basic Information of SLCO4C1|
|Protein Name||Solute carrier organic anion transporter family member 4C1|
|Aliases||OATP-H, Organic anion transporter M1, Solute carrier family 21 member 20|
|Organism||Homo sapiens (Human)|
In the kidney, SLCO4C1 might be the first step in the transport of digoxin and various compounds into the urine. SLCO4C1 transports thyroid hormone, digoxin, endogenous digoxigenin-like compound, and methotrexate. Many compounds accumulate during renal failure, and kidney-specific SLCO4C1 excretes uremic toxins, resulting in reduced blood pressure and kidney inflammation. Human kidney-specific OATP SLCO4C1 is a molecule responsible for excretion of uremic toxins, and its overexpression in rat kidneys can promote renal excretion of uremic toxins, reduce hypertension, heart hypertrophy and inflammation in renal failure. In addition, SLCO4C1 overexpression can decrease plasma levels of the uremic toxins guanidino succinate, asymmetric dimethylarginine, and the newly identified trans-aconitate. Up-regulation of kidney SLCO4C1 promotes excretion of uremic toxins, reduces kidney inflammation, slows the progression of kidney damage and hemodialysis.
Fig.1 Uremic toxins and SLCO4C1 transporter in renal failure. (Suzuki, 2011)
This paper demonstrates that SLCO4C1-mediated excretion of uremic toxins and overexpression of human SLCO4C1 in rat kidney promotes renal excretion of uremic toxins and reduces hypertension, cardiac hypertrophy and renal inflammation in renal failure.
This study finds that drugs that upregulate SLCO4C1 expression may have therapeutic potential for uremic patients.
This article uses OATP4C1-expressing cells to screen 53 clinically representative drugs to study OATP4C1-mediated drug interactions, providing new insights into the role of OATP4C1 in clinical DDI.
This review reports that rat Oatp4c1 flows to the apical cell surface of polarized epithelium and is predominantly localized to the proximal straight tube.
This study describes that any combination of the three OATPs (OATP1B1, OATP1B3, and OATP2B1) can serve as an important drug-drug interaction (DDI) target that alters drug pharmacokinetics, toxicity, and efficacy characteristics of the victim.
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