Association of Caveolin-1 Gene Polymorphism With Kidney Transplant Fibrosis and Allograft Failure

Moore, Jason H.; McKnight, Amy Jayne; Simmonds, Matthew J.; Courtney, Aisling E.; Hanvesakul, Raj; Brand, Stephan; Briggs, David; Ball, Simon; Cockwell, Paul; Patterson, Christopher; Maxwell, Alexander P.; Gough, Stephen; Borrows, Richard

doi:10.1001/jama.2010.356

Cited by 67 publications

(89 citation statements)

References 13 publications

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“…Although the mechanism for the residual fibrosis seen at the atrophic phase is unknown, a role for inactivating mutations in Cav1, the gene coding for the antifibrogenic protein caveolin1, appears possible. 22 Such mutations are associated with increased risk of allograft failure in kidney transplants, 23 whereas caveolin1 deficiency has been linked to human and experimental systemic sclerosis, and to other fibrogenic syndromes. 24 Whereas a mendelian pattern of inheritance has not been determined for PRS, 25,26 the clustering of hemifacial atrophy, morphea, and parotid gland involvement suggests genetic linkage that may perhaps extend to other types of morphea.…”

Section: Discussionmentioning

confidence: 99%

Activity assessment in morphea using color Doppler ultrasound

Wortsman

Sázunic

et al. 2011

Journal of the American Academy of Dermatology

109

161

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Section: Discussionmentioning

confidence: 99%

Activity assessment in morphea using color Doppler ultrasound

Wortsman

Sázunic

et al. 2011

Journal of the American Academy of Dermatology

109

161

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“…80 Moreover, the role of other polymorphically expressed genes, such as, for example, transforming growth factor-b, vascular endothelial growth factor, and caveolin-1 requires further study. [81][82][83] Finally, there is at present only limited evidence that ABCB1 and CYP3A genotype ultimately influence graft (or patient) survival.…”

Section: Discussionmentioning

confidence: 99%

The Pharmacogenetics of Calcineurin Inhibitor–Related Nephrotoxicity

Hesselink

Bouamar²,

Gelder³

2010

Therapeutic Drug Monitoring

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Chronic calcineurin inhibitor (CNI)-induced nephrotoxicity is associated with prolonged use of cyclosporine and tacrolimus and has been observed after all types of transplantation, as well as during treatment of autoimmune disease. Extensive alterations in the renal architecture including glomerular sclerosis, tubular atrophy and interstitial fibrosis may lead to end-stage renal failure. Increasing evidence shows that pharmacogenetic factors explain part of the between-patient differences in susceptibility to developing CNI-induced nephrotoxicity. In this paper this evidence is reviewed, with special emphasis on the role of genetic factors influencing metabolism and transportation of CNIs in both acceptor and donor.

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“…Indeed, one may consider that kidney lesions may be influenced by the genetic background of the kidney (i.e., of the donor), rather than that of the recipient. This approach has been advocated in two recent studies: one that investigated the role of caveolin-1 polymorphisms in kidney transplant fibrosis and allograft failure (Moore et al 2010) and another evaluating Apolipoprotein-1 polymorphisms in African-American donors (Reeves-Daniel et al 2010).…”

Section: Long-term Outcomes and The C3 Paradigmmentioning

confidence: 99%

The genetics of kidney transplantation

Pallet

Thervet

2011

Hum Genet

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Over the last decade, the search for gene variants with the potential to influence transplant outcomes or predispose individuals to host-recipient-related phenotypes has generated a considerable number of studies with conflicting results. Thousands of genotypes have been associated with complex traits related to transplant medicine, including acute rejection, immunosuppressive drug metabolism and side effects, infections, long-term outcomes, and cardiovascular complications. However, these efforts have given disappointing results, both in terms of gaining understanding of the biological basis of disease and in patient management. The methodological weaknesses that constitute the major limitations of most of these studies have been discussed widely. A new generation of approaches is needed to understand the relationship between gene variants and complex kidney transplantation traits. These approaches should be global, to generate original pathophysiological hypotheses, and should rely on advanced genomic tools, including Genome Wide Association studies and Whole Genome Sequencing technologies. Such enterprises will only be successful with the creation of international consortiums that connect partners in clinical, industrial, and academic transplant medicine.

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Association of Caveolin-1 Gene Polymorphism With Kidney Transplant Fibrosis and Allograft Failure

Abstract: Among kidney transplant donors, the CAV1 rs4730751 SNP was significantly associated with allograft failure in 2 independent cohorts.

Cited by 67 publications

References 13 publications

Activity assessment in morphea using color Doppler ultrasound

Activity assessment in morphea using color Doppler ultrasound

The Pharmacogenetics of Calcineurin Inhibitor–Related Nephrotoxicity

The genetics of kidney transplantation

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