Heart-type fatty acid-binding protein (H-FABP) as an early diagnostic biomarker in patients with acute chest pain

Vupputuri, Anjith; Sekhar, Saritha; Krishnan, Sajitha; Venugopal, K.; Natarajan, K

doi:10.1016/j.ihj.2015.06.035

Cited by 42 publications

(30 citation statements)

References 17 publications

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“…Myoglobin, H-FABP, and GP-BB are responsive indicators of cardiomyocyte injuries in the serum. [31] Augmented levels of myoglobin, GP-BB, and H-FABP were found in the serum of DOXtreated cardiotoxic rats in the current study in agreement with the earlier findings, [32,33] whereas, nimbolide treatment decreased H-FABP, myoglobin, and GP-BB levels ( Figure 5).…”

Section: Discussionsupporting

confidence: 92%

Nimbolide prevents myocardial damage by regulating cardiac biomarkers, antioxidant level, and apoptosis signaling against doxorubicin‐induced cardiotoxicity in rats

Xia

Chen

et al. 2020

J Biochem & Molecular Tox

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The current work planned to assess the protecting properties of nimbolide against doxorubicin (DOX)‐treated myocardial damage. Myocardial damage was produced with 2.5 mg/kg of DOX given on alternative days (14 days). Thiobarbituric acid reactive substances (TBARS) levels of a lipid peroxidative marker were elevated, whereas reduced body weight, heart weight, blood pressure indices and reduced levels of antioxidants like glutathione‐S‐transferase, superoxide dismutase, catalase, glutathione peroxidase, glutathione, and glutathione reductase were observed in the heart tissue of DOX‐treated animals. DOX‐treated animals showed augmented levels of cardiac markers likes monocyte chemotactic protein‐1, interferon‐gamma, aspartate transferase, creatine kinase, lactate dehydrogenase, creatine kinase‐muscle/brain, heart‐type fatty acid‐binding protein, glycogen phosphorylase isoenzyme BB, transforming growth factor‐β, brain natriuretic peptide, myoglobin, and cTnI in serum. Histopathological assessment confirmed the DOX‐induced cardiotoxicity. Furthermore, DOX‐induced rats showed augmented inflammatory mediators (nuclear factor‐κB [NF‐kB], tumor necrosis factor‐α [TNF‐α], and interleukin‐1β [IL‐1β]) and increased PI3K/Akt signaling proteins (PI3K, p‐Bad/Bad, caspase‐3, and p‐Akt), whereas decreased oxidative markers (HO‐1 and NQO‐1) and p‐PTEN were observed. Nimbolide‐supplemented rats showed reduced activity/levels of cardiac markers and TBARS levels in serum and heart tissue. Levels of enzymatic and nonenzymatic antioxidants were augmented in the heart tissue of nimbolide‐supplemented rats. Nimbolide influence decreased apoptosis, inflammation, and enhanced antioxidant markers through the modulation of p‐Bad/Bad, caspase‐3, PI3K, p‐Akt, TNF‐α, NF‐kB, IL‐1β, HO‐1, NQO‐1, and p‐PTEN markers. The histopathological explanations were observed to be in line with biochemical analysis. Therefore, the finding of current work was that nimbolide has a defensive effect on the myocardium against DOX‐induced cardiac tissue damage.

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Section: Discussionsupporting

confidence: 92%

Nimbolide prevents myocardial damage by regulating cardiac biomarkers, antioxidant level, and apoptosis signaling against doxorubicin‐induced cardiotoxicity in rats

Xia

Chen

et al. 2020

J Biochem & Molecular Tox

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“…H-FABP is undetectable in normal conditions but is released rapidly from cardiomyocytes into circulating blood after myocardial damage. Previous studies have demonstrated that H-FABP is closely associated with acute coronary syndrome 32 , hypertrophic and dilated cardiomyopathy, heart failure, stroke, obstructive sleep apnea syndrome and pulmonary embolism [14][15][16][17][18][19][20][21] . MI is one of the most serious challenges of contemporary cardiology.…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, H-FABP has been used diagnostic marker for acute coronary syndromes 15 . On the other hand, previous studies have demonstrated that serum level of H-FABP is increased in patients with hypertrophic and dilated cardiomyopathy, heart failure, stroke, obstructive sleep apnea syndrome and pulmonary embolism [13][14][15][16][17][18][19][20][21] .…”

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confidence: 99%

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2017

IJPSR

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“…e addition of hFABP to hs-cTn has more accuracy and accelerates clinical diagnostic decisions by identifying the patients at low risk for AMI [100,101]. Another study has demonstrated that hFABP has superior sensitivity than cTnI and suggests a combination use of hFABP and cTnI subsequently to diagnose AMI [102].…”

Section: Heart-type Fatty Acid Binding Protein (Hfabp)mentioning

confidence: 99%

The Biomarkers for Acute Myocardial Infarction and Heart Failure

Wang

Zhang

et al. 2020

BioMed Research International

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The use of a large number of cardiovascular biomarkers, meant to complement the use of the electrocardiogram, echocardiography cardiac imaging, and clinical symptom assessment, has become a routine in clinical diagnosis, differential diagnosis, risk stratification, and prognosis and guides the management of patients with suspected cardiovascular diseases. There is a broad consensus that cardiac troponin and natriuretic peptides are the preferred biomarkers in clinical practice for the diagnosis of the acute coronary syndrome and heart failure, respectively, while the roles and possible clinical applications of several other potential biomarkers are still under study. This review mainly focuses on the recent studies of the roles and clinical applications of troponin and natriuretic peptides, which seem to be the best-validated markers in distinguishing and predicting the future cardiac events of patients with suspected cardiovascular diseases. Additionally, the review briefly discusses some of the large number of potential markers that may play a more prominent role in the future.

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Heart-type fatty acid-binding protein (H-FABP) as an early diagnostic biomarker in patients with acute chest pain

Cited by 42 publications

References 17 publications

Nimbolide prevents myocardial damage by regulating cardiac biomarkers, antioxidant level, and apoptosis signaling against doxorubicin‐induced cardiotoxicity in rats

Nimbolide prevents myocardial damage by regulating cardiac biomarkers, antioxidant level, and apoptosis signaling against doxorubicin‐induced cardiotoxicity in rats

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The Biomarkers for Acute Myocardial Infarction and Heart Failure

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