Cellular and molecular mechanisms in pulmonary hypertension – Tran Lundmark

Pulmonary hypertension (PH) is a life‐threatening condition, which untreated leads to right heart failure and death. The disease is characterized by three major pathological changes in the pulmonary arterial wall: 1) vasoconstriction, 2) cell proliferation and remodeling, and 3) in situ thrombosis. Current treatment with prostaglandin analogues, nitric oxide, endothelin receptor antagonists, and phosphodiesterase‐5 inhibitors, target mainly the vasoconstrictive component and provide limited improvement of symptoms and prognosis. Perlecan and versican, two proteoglycans in extracellular matrix, are important regulators of smooth muscle cell proliferation in peripheral vascular disease, but their role in the pulmonary vasculature is unknown. Our hypothesis is that perlecan is inhibitory while versican is stimulatory for the proliferation of pulmonary artery smooth muscle cells (paSMC). Our aim is therefore to investigate the role of perlecan and versican in the regulation of the proliferative component of PH; and to evaluate the efficacy of experimental drugs that alter the levels of perlecan and versican in pulmonary arteries.


Om du skulle vilja stödja detta forskningsområde kan du göra det via följande konton:

BG 628-4418
PG 514114-8
Ange: Karin Tran Lundmark

Om du befinner dig utanför Sverige, vänligen använd följande information:

Bank: SEB, Stockholm, Sweden
Kontonummer: 5201-11 370 12
Iban-nummer: SE16 5000 0000 0520 1113 7012
Bic-kod (bankens elektroniska adress): ESSESESS
Kontoinnehavare: Stiftelsen Centrum för Molekylär Medicin
L8:05, Karolinska Universitetssjukhuset
171 76 Stockholm, Sweden

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