Inflammation and chronic heart failure: From biomarkers to novel anti-inflammatory therapeutic strategies

Επιστημονική δημοσίευση - Άρθρο Περιοδικού uoadl:3061014 15 Αναγνώσεις

Μονάδα:
Ερευνητικό υλικό ΕΚΠΑ
Τίτλος:
Inflammation and chronic heart failure: From biomarkers to novel anti-inflammatory therapeutic strategies
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Heart failure (HF) is a complex heterogeneous syndrome with immune, metabolic and neurohumoral mechanisms interacting and leading to gradual heart contractility impairment. From the first study- to correlate inflammation with HF, inflammation biomarkers have been the subject of intense inquiry in patients with various forms of HF. Chronic HF (CHF) is strongly associated with inflammation in terms of pathogenesis, progression, severity and prognosis. Inflammatory mediators participate in CHF pathophysiology in various ways like exerting direct impact on cardiac myocytes, fibroblasts and β-adrenergic receptors leading to hypertrophy, fibrosis and impaired cardiac contractility, respectively, or inducing apoptosis by stimulation of the proper genes. The anti-inflammatory effects of classical heart failure therapeutic strategies such as ACEI and b-blockers are rather conflicting. Whether novel immunomodulating and anti-inflammatory therapeutic approaches should be added to existing therapies in order to ensure additional benefit to HF patients is under investigation. In this review, we summarize the pathophysiological link between inflammatory processes and CHF, focusing on the role of novel and traditional inflammatory biomarkers and highlighting novel anti-inflammatory therapeutic strategies.
Έτος δημοσίευσης:
2014
Συγγραφείς:
Bouras, G.
Giannopoulos, G.
Hatzis, G.
Alexopoulos, D.
Leventopoulos, G.
Deftereos, S.
Περιοδικό:
RSC Medicinal Chemistry
Εκδότης:
Bentham Science Publishers
Τόμος:
10
Αριθμός / τεύχος:
7
Σελίδες:
682-689
Λέξεις-κλειδιά:
angiotensin receptor antagonist; antiinflammatory agent; azathioprine; beta adrenergic receptor blocking agent; biological marker; C reactive protein; candesartan; carvedilol; colchicine; digoxin; dipeptidyl carboxypeptidase inhibitor; diuretic agent; etanercept; galectin 3; glucocorticoid; hydroxymethylglutaryl coenzyme A reductase inhibitor; immunomodulating agent; infliximab; losartan; metalloproteinase; methotrexate; metoprolol; myeloperoxidase; olmesartan; omega 3 fatty acid; osteoprotegerin; rosuvastatin; telmisartan; thalidomide; valsartan; biological marker; nonsteroid antiinflammatory agent, antiinflammatory activity; apoptosis; Article; disease association; disease course; disease severity; fibroblast; fibrosis; gene; heart failure; heart muscle cell; heart muscle contractility; human; hypertrophy; inflammation; nonhuman; pathogenesis; pathophysiology; priority journal; prognosis; animal; chemistry; chronic disease; complication; heart failure; inflammation; metabolism; synthesis, Animals; Anti-Inflammatory Agents, Non-Steroidal; Biological Markers; Chronic Disease; Heart Failure; Humans; Inflammation
Επίσημο URL (Εκδότης):
DOI:
10.2174/1573406410666140318113325
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