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Table 1 Main objectives of the 24 articles eligible for inclusion in this review

From: Association between CYP3A4/CYP3A5 genetic polymorphisms and treatment outcomes of atorvastatin worldwide: is there enough research on the Egyptian population?

S.no

Author (s)

Main Objective (s)

1

Dagli-Hernandez et al. [15]

To review clinical trials on pharmacogenomics of statins regarding the Brazilian population

2

Rosales et al. [21]

To evaluate the response to atorvastatin in Chilean hypercholesterolemic patients with PMsa in ABCB1b, CYP3A5c, and CYP3A4c genes

3

Shitara, Sugiyama. [24]

To review statins' PKd and physicochemical issues and specific aspects such as PMsa that could affect PKd

4

Kivistö et al. [25]

To investigate whether CYP3A5c expression results in poor response to statin therapy in Caucasians

5

Zubiaur et al. [26]

To evaluate the impact of SLCO1B1e phenotype on atorvastatin exposure by conducting a candidate gene pharmacogenetic research

6

He et al. [27]

To assess the influence of CYP3A4*1Gc variant on atorvastatin PKd in China's Han subjects with CADf

7

Park et al. [28]

To evaluate the contributions of CYP3A5c and CYP3A4c to atorvastatin metabolism

8

Maekawa et al. [29]

To assess, in vitro, the influence of CYP3A4*18c and CYP3A4*16c on the enzymatic function required for the metabolism of several drugs, including atorvastatin

9

Jani et al. [30]

To investigate CYP450c genetic PMsa among Gujarat subjects in India depending on atorvastatin as a probe

10

Poduri et al. [31]

To examine the influence of PMsa of six specific genes on the therapeutic effect of statins in subjects suffering CADf

11

Gao et al. [32]

To investigate the influence of CYP3A4*1Gc PMa on statins therapy

12

Peng et al. [33]

To illustrate the association between CYP450c genetic PMsa and response to atorvastatin in Chinese patients with ischemic stroke

13

Kajinami et al. [34]

To study the effect of three CYP3A4c variant alleles on atorvastatin treatment

14

Willrich et al. [35] 

To summarize findings from previous studies on variations in responses to statins due to CYP3Ac PMsa

15

Kadam et al. [36]

To screen LDL-Cg level after atorvastatin treatment in Indian carriers of genetic PMsa in several enzymes involved in the pharmacodynamics and PKd of statins

16

Klein et al. [37]

To examine the effect of genetic mutations on the phenotype of CYP3A4c in human hepatocytes and participants using atorvastatin

17

Kolovou et al. [38]

To investigate the effect of CYP3A5*3c PMsa on the lipid profile after atorvastatin or simvastatin treatment

18

Willrich et al. [39]

To assess the impact of CYP3A5c PMsa on statins efficacy in 139 hypercholesterolemic Brazilians

19

Vrablik et al. [40]

To review literature about statin-induced myopathy

20

Becker et al. [41]

To investigate the influence of CYP3A4c and ABCB1b PMsa on intolerance to atorvastatin or simvastatin treatment

21

Xia et al. [42]

To develop and validate a UHPLC-MS/MSh approach for studying atorvastatin calcium PKd in healthy carriers of certain genotypes

22

Liu et al. [43]

To explore the impact of microRNA on the inherited malfunctioning CYP3A4/5c enzymes and atorvastatin metabolism

23

Wilke et al. [44]

To investigate the assumption that carriers of CYP3A5*3c or CYP3A4*1Bc are at risk of myopathy due to atorvastatin

24

Benes et al. [45]

To review the risks for ADRsi of commonly recommended statins

  1. a. (PMs): polymorphisms, b. (ABCB1): ATP-binding cassette transporter B1, c. (CYP): Cytochrome P450 enzyme, d. (PK): pharmacokinetics, e. (SLCO1B1): solute carrier organic anion transporter family member 1B1, f.(CAD): coronary artery disease, g.(LDL-C): low-density lipoprotein-cholesterol, h. (UHPLC-MS/MS): ultra-high-performance liquid chromatography coupled with tandem triple quaternary mass spectrometry, i. (ADRs): adverse drug reactions