Cystatin <scp>C</scp>: A potential biomarker for pulmonary arterial hypertension

Fenster, Brett E.; Lasalvia, Luis; Schroeder, Joyce; Smyser, Jamey; Silveira, Lori; Buckner, J. Kern; Brown, Kevin K.

doi:10.1111/resp.12259

Cited by 25 publications

(23 citation statements)

References 38 publications

(57 reference statements)

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“…The inflammatory derived mediators (e.g., GM-CSF, ICAM-1, IL-6, and RANTES) are mainly responsible for increased accumulation and activation of immune cells within the site of inflammation [1]. Interestingly, the high levels of angiogenin and cystatin in plasma of patients are believed to represent the potential biomarkers for PH [62,63]. Besides that, EMMPRIN and PDGF were also shown to be associated with the pathogenesis of various lung diseases [62,64].…”

Section: Discussionmentioning

confidence: 99%

Asymmetric dimethyl arginine induces pulmonary vascular dysfunction via activation of signal transducer and activator of transcription 3 and stabilization of hypoxia-inducible factor 1-alpha

Pekarová

Koudelka

Kolářová

et al. 2015

Vascular Pharmacology

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Section: Discussionmentioning

confidence: 99%

Asymmetric dimethyl arginine induces pulmonary vascular dysfunction via activation of signal transducer and activator of transcription 3 and stabilization of hypoxia-inducible factor 1-alpha

Pekarová

Koudelka

Kolářová

et al. 2015

Vascular Pharmacology

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“…В нашем исследовании мы продемонстрировали тесную связь между ЛГ и уровнем цистатина С в сыворотке крови. В небольшом исследовании у 14 больных с ЛАГ и сохранной функцией почек отмечалось повышение уровня цистатина С по сравнению с контролем [23]. Данный биомаркер коррелировал со структурными и функциональными параметрами ПЖ сердца.…”

Section: Discussionunclassified

Risk factors for pulmonary hypertension at the predialysis stage of chronic kidney disease

et al. 2016

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“…red cell distribution width -RDW) and microRNAs (e.g. microRNA-150) [6,93,[95][96][97][98][99][100][101][102][103][104][105]. The possibility that factors that report on different components of the pathology of PAH might be combined to better effect merits careful evaluation.…”

Section: Circulating Biomarkersproviding Insight Into the Disease Andmentioning

confidence: 99%

Pulmonary arterial hypertension – progress in understanding the disease and prioritizing strategies for drug development

et al. 2017

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Abstract. Ghataorhe P, Rhodes CJ, Harbaum L, Attard M, Wharton J, Wilkins MR (Imperial College London, London, UK). Pulmonary arterial hypertensionprogress in understanding the disease and prioritizing strategies for drug development (Review). J Intern Med 2017; 282: 129-141.Pulmonary arterial hypertension (PAH), at one time a largely overlooked disease, is now the subject of intense study in many academic and biotech groups. The availability of new treatments has increased awareness of the condition. This in turn has driven a change in the demographics of PAH, with an increase in the mean age at diagnosis. The diagnosis of PAH in more elderly patients has highlighted the need for careful phenotyping of patients and for further studies to understand how best to manage pulmonary hypertension associated with, for example, left heart disease. The breadth and depth of expertise focused on unravelling the molecular pathology of PAH has yielded novel insights, including the role of growth factors, inflammation and metabolic remodelling. The description of the genetic architecture of PAH is accelerating in parallel, with novel variants, such as those reported in potassium two-pore domain channel subfamily K member 3 (KCNK3), adding to the list of more established mutations in genes associated with bone morphogenetic protein receptor type 2 (BMPR2) signalling. These insights have supported a paradigm shift in treatment strategies away from simply addressing the imbalance of vasoactive mediators observed in PAH towards tackling more directly the structural remodelling of the pulmonary vasculature. Here, we summarize the changing clinical and molecular landscape of PAH. We highlight novel drug therapies that are in various stages of clinical development, targeting for example cell proliferation, metabolic, inflammatory/immune and BMPR2 dysfunction, and the challenges around developing these treatments. We argue that advances in the treatment of PAH will come through deep molecular phenotyping with the integration of clinical, genomic, transcriptomic, proteomic and metabolomic information in large populations of patients through international collaboration. This approach provides the best opportunity for identifying key signalling pathways, both as potential drug targets and as biomarkers for patient selection. The expectation is that together these will enable the prioritization of potential therapies in development and the evolution of personalized medicine for PAH.

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Cystatin C: A potential biomarker for pulmonary arterial hypertension

Abstract: In a small cohort, CysC accurately correlates with RV pressure, function and morphology. CysC may represent a novel PAH biomarker.

Cited by 25 publications

References 38 publications

Asymmetric dimethyl arginine induces pulmonary vascular dysfunction via activation of signal transducer and activator of transcription 3 and stabilization of hypoxia-inducible factor 1-alpha

Asymmetric dimethyl arginine induces pulmonary vascular dysfunction via activation of signal transducer and activator of transcription 3 and stabilization of hypoxia-inducible factor 1-alpha

Risk factors for pulmonary hypertension at the predialysis stage of chronic kidney disease

Pulmonary arterial hypertension – progress in understanding the disease and prioritizing strategies for drug development

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