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Heart fatty acid-binding protein (H-FABP) belongs to a family of intracellular fatty acid-binding proteins that are involved in the transport of long-chain fatty acids. Previous studies have indicated that H-FABP is significantly associated with intramuscular fat (IMF) content in pig. In this study, we compared the mRNA and protein expression of H-FABP between Tibetan pig (with high IMF) and Large White pig (with low IMF). The expression of H-FABP at both mRNA and protein levels in the tissues of backfat, longissimus dorsi muscle and liver was found to be significantly higher in TP than in LW. Single-nucleotide polymorphisms (SNPs) in a 2 kb region upstream of the start codon of the gene were screened using Sanger sequencing. We accordingly identified three SNPs (C-1375G, C-314T and T-158G) between the TP and LW populations and genotyped these based on PCR-restriction fragment length polymorphisms (PCF-RFLPs) analysis. The results showed that the C-1375G site might regulate H-FABP gene expression and thus be associated with fat deposition in pigs. Our study provides important data for further investigating the regulatory mechanism of H-FABP for fat deposition in pigs., (Copyright © 2019 Elsevier B.V. All rights reserved.)

The current clinical care of glioblastomas leaves behind invasive, radio- and chemo-resistant cells. We recently identified mammary-derived growth inhibitor (MDGI/ FABP3 ) as a biomarker for invasive gliomas. Here, we demonstrate a novel function for MDGI in the maintenance of lysosomal membrane integrity, thus rendering invasive glioma cells unexpectedly vulnerable to lysosomal membrane destabilization. MDGI silencing impaired trafficking of polyunsaturated fatty acids into cells resulting in significant alterations in the lipid composition of lysosomal membranes, and subsequent death of the patient-derived glioma cells via lysosomal membrane permeabilization (LMP). In a preclinical model, treatment of glioma-bearing mice with an antihistaminergic LMP-inducing drug efficiently eradicated invasive glioma cells and secondary tumours within the brain. This unexpected fragility of the aggressive infiltrating cells to LMP provides new opportunities for clinical interventions, such as re-positioning of an established antihistamine drug, to eradicate the inoperable, invasive, and chemo-resistant glioma cells from sustaining disease progression and recurrence., (© 2019 The Authors. Published under the terms of the CC BY 4.0 license.)

Fatty acid-binding protein 3 (FABP3), a low-molecular-weight protein, participates in lipid transportation, storage, signaling transduction, oxidation, and transcription regulation. Here, we investigated the expression and function of FABP3 in ischemic heart diseases and explored the mechanisms by which FABP3 affected remodeling after myocardial infarction (MI). We showed that ischemic or hypoxic conditions upregulated FABP3 expression in vivo and in vitro. Notably, overexpression of FABP3 induced more myocyte apoptosis in the infarction and border areas and aggravated cardiac dysfunction, with lower left ventricular ejection fraction. Meanwhile, overexpression of FABP3 drastically promoted death and apoptosis of neonatal rat ventricular cardiomyocytes under hypoxia. Furthermore, deficiency of FABP3 exerted protective effects against ischemic heart injuries by decreasing cardiac myocyte apoptosis and heart remodeling after MI. We found that overexpression of FABP3 upregulated the phosphorylation of MAPK signaling pathway and decreased phosphorylated Akt levels, which may account for the augmentation of apoptosis and remodeling after MI. To the best of our knowledge, this is the first study to demonstrate that deficiency of FABP3 would protect cardiac myocytes from apoptosis and alleviate cardiac remodeling after MI, suggesting FABP3 as a potential target to preserve cardiac function after MI. NEW & NOTEWORTHY It is an undisputable fact that myocyte apoptosis plays a crucial role in cardiac remodeling and the development of heart failure after myocardial infarction. Here, fatty acid-binding protein 3 deficiency improved myocardial structural remodeling and function by decreasing cell apoptosis and regulating MAPK signaling pathways. We suppose that fatty acid-binding protein 3 may be regarded as a potential intervention approach to preserve cardiomyocytes during myocardial infarction.

Aims: The importance of true worsening renal failure (WRF), which is associated with a poor prognosis, had been suggested in patients with acute heart failure (AHF). The aim of the present study was to establish the biomarker strategy for the prediction of true WRF in AHF., Methods and Results: Two hundred eighty-one patients with AHF were analysed. Their biomarkers were measured within 30 min of admission. Patients were assigned to the non-WRF (n = 168), pseudo-WRF (n = 56), or true-WRF (n = 57) groups using the criteria of both acute kidney injury on admission and increasing serum creatinine value during the first 7 days. A Kaplan-Meier curve showed that the survival and heart failure event rate of the true-WRF group within 1000 days was significantly lower than that of the non-WRF and pseudo-WRF groups (P ≤ 0.001). The multivariate Cox regression model also indicated that true WRF was an independent predictor of 1000 day mortality and heart failure events [hazard ratio: 4.315, 95% confidence interval (CI): 2.466-7.550, P ≤ 0.001, and hazard ratio: 2.834, 95% CI: 1.893-4.243, P ≤ 0.001, respectively]. The serum heart-type fatty acid-binding protein (s-HFABP) levels were significantly higher in the true-WRF group than in the non-WRF and pseudo-WRF groups (P ≤ 0.001). The multivariate logistic regression model indicated that the predictive biomarker for the true-WRF group was the s-HFABP level (odds ratio: 5.472, 95% CI: 2.729-10.972, P ≤ 0.001). The sensitivity and specificity for indicating the presence of true WRF were 73.7% and 76.8% (area under the curve = 0.831) for s-HFABP in whole patients, respectively, and 94.7% and 72.7% (area under the curve = 0.904) in non-chronic kidney disease (CKD) patients, respectively., Conclusions: Cardiac biomarkers, especially the s-HFABP, might predict the development of true WRF in AHF patients. Furthermore, the predictive value was higher in AHF patients without CKD than in those with CKD., (© 2019 The Authors ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.)

It is accepted that smaller mammals with higher metabolic rates have shorter lifespans. The very few species that do not follow these rules can give insights into interesting differences. The recorded maximum lifespans of bats are exceptional - over 40 years, compared with the laboratory mouse of 4 years. We investigated the differences in the biochemical composition of mitochondria between bat and mouse species. We used proteomics and ultra-high-performance liquid chromatography coupled with high resolution mass spectrometry lipidomics, to interrogate mitochondrial fractions prepared from Mus musculus and Pipistrellus pipistrellus brain and skeletal muscle. Fatty acid binding protein 3 was found at different levels in mouse and bat muscle mitochondria and its orthologues were investigated in Caenorhabditis elegans knock-downs for LBP 4, 5 and 6. In the bat, high levels of free fatty acids and N-acylethanolamine lipid species together with a significantly greater abundance of fatty acid binding protein 3 in muscle (1.8-fold, p =0.037) were found. Manipulation of fatty acid binding protein orthologues in C. elegans suggest these proteins and their role in lipid regulation are important for mitochondrial function.

In Parkinson's disease (PD), α-synuclein (αSyn) accumulation and inclusion triggers dopamine neuronal death and synapse dysfunction in vivo. We previously reported that fatty acid-binding protein 3 (FABP3) is highly expressed in the brain and accelerates αSyn oligomerization when cells are exposed to 1-Methyl-1,2,3,6-tetrahydropiridine (MPTP). Here, we demonstrate that αSyn oligomerization was markedly enhanced by co-overexpressing FABP3 in neuro-2A cells when cells were treated with arachidonic acid (AA). We developed FABP3 ligands, which bind to the fatty acid binding domain of FABP3, using an 8-Anilinonaphthalene-1-sulfonic acid (ANS) assay with a recombinant FABP3 protein. The prototype for the FABP4 ligand, BMS309403, has no affinity for FABP3. We developed more FABP3-specific ligands derived from the chemical structure of BMS309403. Like AA, ligands 1, 7, and 8 had a relatively high affinity for FAPB3 in the ANS assay. Then, we evaluated the inhibition of αSyn oligomerization in neuro-2A cells co-overexpressing FABP3 and αSyn. Importantly, AA treatments markedly enhanced αSyn oligomerization in the co-expressing cells. Ligands 1, 7, and 8 significantly reduced AA-induced αSyn oligomerization in neuro-2A cells. Taken together, our results indicate that FABP3 ligands that target FABP3 may be used as potential therapeutics that inhibit αSyn aggregation in vivo., (Copyright © 2018 Elsevier B.V. All rights reserved.)

The study objective was to investigate heart-fatty acid binding protein (HFABP) concentrations in dogs with degenerative valvular disease (MVD) and dilated cardiomyopathy (DCM), and its potential as a prognostic factor. Plasma HFABP, N-terminal pro brain natriuretic peptide (NTproBNP) and serum cardiac troponin I (cTnI) levels were measured in 21 control dogs, 23 dogs with MVD and 13 dogs with DCM, with repeated sampling at 1 and 3 months after initial presentation. All dogs were followed up after 6 and 12 months to verify survival. Heart-fatty acid binding protein concentrations were significantly higher in dogs with MVD and DCM than controls at initial presentation, and after 1 month in dogs with MVD. For dogs with DCM, a significant reduction in HFABP levels over time was observed. Comparing ACVIM stages, highest HFABP concentrations were detected in ACVIM stage C dogs compared to stage B, with the lowest levels seen in controls, and a reduction over time in stage C dogs was present. Similarly, cTnI concentrations were higher in DCM and stage C in comparison to control dogs and reduced over time, while NTproBNP concentrations were only higher in diseased dogs at 1 month. Heart-fatty acid binding protein and cTnI levels at initial presentation and ACVIM disease stage were independent predictors of survival in a univariate analysis. The elevation of HFABP in dogs with MVD and DCM in comparison to controls, its association with disease severity, and its potential in predicting reduced survival, suggest that HFABP might be useful as marker for canine MVD and DCM., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

The aim of this study was to determine the effects of isonitrogenous and isocaloric diets containing different qualities of forages and concentrate content on milk fat composition and genes that encode mammary lipogenic enzymes in dairy cows. A total of 20 Holstein cows were assigned to 1 of 2 treatment diets composed of either mixed forages (MF, starch : 21.50%) or corn stover forage (CS, starch : 25.39%). Mammary tissue biopsies were performed to analyze the mRNA expression of lipogenic enzymes. Dry matter intake, body weight, milk protein, and lactose were not affected by treatments. The milk yield, fat content and saturated fatty acid (SFA) and short- and medium-chain fatty acid (SMFA) contents in milk were lower in the CS diet than in the MF diet, but the unsaturated FA and long-chain FA contents were higher. Genes involved in de novo FA synthesis, FA uptake and transport, and Δ9-desaturation were lower in the CS treatment than in the MF treatment. No effects on the nuclear transcription factors were observed between the two treatments. The data indicated that corn stover diet reduced the milk yield, fat content, SMFA, and SFA contents in milk, as well as the gene expression of mammary lipogenic enzymes in dairy cows., (© 2018 Japanese Society of Animal Science.)

Strength exercise is a strategy applied in sports and physical training processes. It may induce skeletal muscle hypertrophy. The hypertrophy is dependent on the eccentric muscle actions and on the inflammatory response. Here, we evaluate the physiological, immunological, and inflammatory responses induced by a session of strength training with a focus on predominance of the eccentric muscle actions. Twenty volunteers were separated into two groups: the untrained group (UTG) and the trained group (TG). Both groups hold 4 sets of leg press, knee extensor, and leg curl at 65% of personal one-repetition maximum (1RM), 90 s of recovery, and 2 ″ conc/3 ″ eccen of duration of execution in each repetition. Blood samples were collected immediately before and after, 2 hours after, and 24 h after the end of the exercise session. The single session of strength training elevated the heart rate (HR), rating of perceived exertion (RPE), visual analog scale (VAS), and lactate blood level in UTG and TG. Creatine kinase (CK) levels were higher at 2 and 24 h after the end of the exercise in UTG and, in TG, only at 24 h. The number of white blood cells (WBC) and neutrophils increased in UTG and TG, post and 2 h after exercise. Lymphocytes increased postexercise but reduced 2 h after exercise in both groups, while the number of monocytes increased only immediately after the exercise session in UTG and TG. The strength training session elevated the levels of apelin and fatty acid-binding proteins-3 (FABP3) in both groups and brain-derived neurotrophic factor (BDNF) in TG. The single exercise session was capable of inducing elevated HR, RPE, lactate level, and CK levels. This protocol changed the count/total number of circulating immune cells in both groups (UTG and TG) and also increased the level of plasmatic apelin, BDNF, and FLTS1 only in TG and FABP3 myokines in both groups.

We previously reported that fatty acid-binding protein 3 (FABP3) knockout (Fabp3 -/- ) mice exhibit abnormal dopamine-related behaviors such as enhanced dopamine D2 receptor antagonist-induced catalepsy behaviors. Here, we report that Fabp3 null mice exhibit cognitive deficits, hyperlocomotion and impaired fear extinction, and thus show post-traumatic stress disorder (PTSD)-like behaviors. Notably, chronic administration of ramelteon (1.0 mg/kg, p.o.), a melatonin receptor agonist, improved all PTSD-like behaviors tested in Fabp3 -/- mice. Relevant to mechanisms underlying impaired fear extinction, we observed significantly reduced levels of Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) autophosphorylation without changes in ERK phosphorylation in the anterior cingulate cortex (ACC). Inversely, CaMKII autophosphorylation increased in the basolateral amygdala (BLA) but remained relatively unchanged in hippocampus of Fabp3 -/- mice. Likewise, the number of c-Fos-positive neurons in BLA significantly increased after exposure to contextual fear conditions but remained unchanged in the central nucleus of the amygdala (CeA). Importantly, chronic ramelteon administration (1.0 mg/kg, p.o.) restored abnormal c-Fos expression and CaMKII autophosphorylation in the ACC and BLA of Fabp3 -/- mice. Finally, the melatonin receptor antagonist luzindole (2.5 mg/kg, i.p.) blocked ramelteon-dependent improvements. Taken together, Fabp3 -/- mice show PTSD-like behaviors, and ramelteon is a likely attractive candidate for PTSD therapy.

Inactivated mycobacterium phlei (M. phlei) is well known for its immune-stimulatory functions in humans and livestock, but less information is available about the influence on meat quality of pigs when used as a feed additive. This study was designed to evaluate the effects of inactivated M. phlei on growth performance as well as meat quality of fattening pigs. A total of 240 cross-bred pigs ([Landrace × Yorkshire] × Duroc) with initial body weight of 80.14 ± 0.29 kg were randomly allocated to five treatments, each of which consisted of eight replicates with 6six pigs per replicate. The basal diet supplemented with five levels of inactivated M. phlei preparations (0, 3.5 × 10 9 [0.1% w/w], 7 × 10 9 [0.2%], 1.4 × 10 10 [0.4%] or 2.1 × 10 10 [0.6%] colony-forming units/kg) was respectively fed to the control group and four treatment groups for 30 days. Adding 0.4% of inactivated M. phlei to diet increased the average daily feed intake and average daily gain of pigs. Importantly, intramuscular fat percentage in the Longissimus dorsi (LD) was increased by feeding diet containing 0.2%, 0.4% and 0.6% of inactivated M. phlei, despite the pH value, drip loss, cooking loss and filter paper fluid uptake not being influenced. Analysis of the fatty acid components showed that some saturated fatty acids were decreased in LD after feeding inactivated M. phlei, but some monounsaturated fat acids (MUFAs) and polyunsaturated fatty acids were increased (PUFAs), which induced the total contents of MUFAs and PUFAs were improved. RT-PCR assay revealed that feeding inactivated M. phlei up-regulated genes implicated in fat metabolism in muscle, including ELOVL6, FASN, SCD1 and H-FABP. This study revealed that feeding inactivated M. phlei not only increased growth performance of fattening pigs, but also improved the meat quality by increasing intramuscular fat content, thus inactivated M. phlei probably has high utilization value in modern pig production., (© 2018 Japanese Society of Animal Science.)

The purpose of this study was to define the relationship between cardiac depression and morphological and immunological alterations in cardiac tissue after multiple trauma. However, the mechanistic basis of depressed cardiac function after trauma is still elusive. In a porcine polytrauma model including blunt chest trauma, liver laceration, femur fracture and haemorrhage serial trans-thoracic echocardiography was performed and correlated with cellular cardiac injury as well as with the occurrence of extracellular histones in serum. Postmortem analysis of heart tissue was performed 72 h after trauma. Ejection fraction and shortening fraction of the left ventricle were significantly impaired between 4 and 27 h after trauma. H-FABP, troponin I and extracellular histones were elevated early after trauma and returned to baseline after 24 and 48 h, respectively. Furthermore, increased nitrotyrosine and Il-1β generation and apoptosis were identified in cardiac tissue after trauma. Main structural findings revealed alteration of connexin 43 (Cx43) and co-translocation of Cx43 and zonula occludens 1 to the cytosol, reduction of α-actinin and increase of desmin in cardiomyocytes after trauma. The cellular and subcellular events demonstrated in this report may for the first time explain molecular mechanisms associated with cardiac dysfunction after multiple trauma.

In this study, we investigated the genetic variation within 3'UTR of Mammary-Derived Growth Inhibitor (MDGI) gene of buffalo using PCR-SSCP and sequencing; and also analyzed association of polymorphism with the milk production traits. The study revealed two conformational patterns, 'A' and 'B' among 234 Mehsana buffaloes maintained with their records in the field and at farm. The frequency of SSCP variant 'A' was found to be invariably high in the buffalo population under study. Further, association analysis of SSCP variants with various milk production and milk quality traits indicated no significant effect on any of the traits investigated. Sequencing of SSCP variant 'A' showed homozygous G/G and A/A and 'B' had heterozygous G/C and A/G at positions +124 and +140 respectively, in the 3'UTR of buffalo MDGI. The preliminary results showed the substantial variations in the distribution of SSCP variants' frequencies within Mehsana buffaloes, however these variants had non-significant association with milk yield, fat yield and fat percentage in Mehsana buffaloes., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

The molecular mechanisms on milk fat depression (MFD) in response to trans-10,cis-12-conjugated linoleic acid (t10,c12-CLA) supplementation in ruminants were elucidated in this research with dairy goats. A total of 30 2-year-old Xinong Saanen dairy goats [40 ± 5 days in milk (DIM)] at peak lactation stage were assigned to a 3 × 3 Latin square design (14 day treatment period, followed with 14 day washout). Three CLA treatments included (a) control, fed the basal diet only without CLA supplementation; (b) orally supplemented with 8 g/day of lipid-encapsulated CLA (low dose, CLA-1); and (c) orally supplemented with 16 g/day of lipid-encapsulated CLA (high dose, CLA-2). Expression levels of fatty acid metabolism genes in the mammary tissues were analyzed by real-time quantitative polymerase chain reaction (RT-qPCR) in three goats on day 1 and the other three goats on day 14 in each group after the discontinuation of CLA treatment in the third experimental period. Dietary supplementation of CLA led to a significant decrease of milk fat compared to the control (p < 0.05). Milk fat concentrations in CLA-1 and CLA-2 groups were 2.74 and 2.42%, respectively, while the milk fat concentration in the control group was 2.99%. Decreases in short- and medium-chain fatty acids (<16 carbons) and increases in unsaturated fatty acids were observed in the CLA-2 group (p < 0.05). The desaturation indexes of C16 and C18 fatty acids were obviously increased (p < 0.01). RT-qPCR results revealed decreases of the mRNA expression levels of SREBF1, PPARG, LPL, CD36, FABP3, ACSL1, FASN, ACACA, DGAT2, TIP47, ADRP, and BTN1A1 genes in mammary glands (p < 0.05) and an increase of the SCD gene because of CLA supplementation (p < 0.05). In conclusion, t10,c12-CLA-induced MFD was possibly the result from the downregulation of genes involved in lipogenesis in goat mammary glands.

Skeletal muscle (SKM) injury or myopathy results in structural or functional defects in SKMs that can be caused by variety of factors such as (1) genetic, (2) drug-induced, (3) disease progression (cachexia), or (4) aging (sarcopenia). Creatine kinase (CK) and aspartate transaminase (AST) activity assays have been routinely used as SKM injury biomarkers, but they lack sensitivity and tissue specificity. In collaboration with the Predictive Safety Testing Consortium, we evaluated the diagnostic performance of a muscle injury biomarker panel (MIP) compared to CK and AST and their correlation with the histology scores across 34 different rat studies. The MIP panel included the analytes skeletal troponin I, myosin light chain 3, fatty acid binding protein 3, and a CK mass (versus activity) assay. The area under the receiver operator characteristic curve for MIP panel ranged from 0.82 to 0.91 as compared to 0.71 and 0.82 for CK and AST activity assays, respectively. Because the MIP biomarkers outperformed the routine biomarkers, the European Medicines Agency and U.S. Food and Drug Administration posted Letters of Support encouraging further study of these analytes and acknowledged the utility of the MIP panel. Ongoing efforts are directed toward the application of the MIP panel biomarkers in clinical studies and regulatory qualification.

Acute myocardial ischemia is the most common cause of sudden cardiac death. The diagnosis of early myocardial ischemia is a hot point in forensic medicine, which is also an early and important part for a prevention against myocardial infarction. This paper conducts a comprehensive discussion of the structure, function, clinical value and forensic medicine application prospect of ischemia modified albumin （IMA） and heart-type fatty acid binding protein （H-FABP), aiming to determine whether the two proteins can be used as biochemical detection indicators of early myocardial ischemia for the diagnosis of sudden cardiac death in forensic medicine., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Forensic Medicine.)

Oocytes that undergo in vitro maturation (IVM) are metabolically abnormal and accumulate excess lipid content. However, the mechanism of lipid accumulation and the role of cumulus cells in this process are unclear. Recently, it was shown that fatty acid binding proteins (FABPs) performed intra- and extracellular fatty acid transport. We postulated that FABP3 might be responsible for fatty acid transport from cumulus cells to the oocytes via transzonal projections (TZPs) during IVM. Transcript and protein levels of FABP3 were analyzed in both in vivo- and in vitro-matured cumulus-oocyte-complexes and were increased in IVM samples. Further analysis showed increased lipid content in oocytes and cumulus cells in IVM samples compared to in vivo-derived. We therefore speculated that altered traffic of fatty acids via FABP3 during IVM was the mechanism leading to the excess of lipids accumulated within IVM oocytes. Furthermore, we demonstrated an increase in FABP3 levels and lipid content during the first 9 h of IVM, further strengthening the possibility of fatty acid transport via FABP3 and TZPs. Additionally, disruptions of TZPs during IVM decreased lipid accumulation in oocytes. Our results shed light on a possible mechanism involving FABP3 and TZPs that causes excess lipid accumulation in oocytes during IVM.

Cellular uptake of long chain fatty acids in human placental trophoblasts is thought to be mediated by several membrane- and cytoplasmic fatty acid-binding proteins (FABP). FABP3 was shown to be involved in long chain polyunsaturated fatty acids (LCPUFA) uptake in human trophoblastic choriocarcinoma cells, BeWo as the uptake of arachidonic acid,20:4n-6 (ARA) was decreased in FABP3-knockdown BeWo cells. However, the regulation of expression of FABP3 in these cells is not yet well known. The aim of the present study was to examine the FABP3 expression by LCPUFAs, insulin and LXR agonists in BeWo cells. Among all these fatty acids tested, only ARA dose-dependently stimulated the expression of FABP3 protein in these cells after 24h incubation while other fatty acids had no such effect. In addition, LXR agonist and insulin dose-dependently increased FABP3 protein expression in these cells after 24h incubation. Insulin-stimulated FABP3 protein expression was accompanied with an increased arachidonic acid uptake. Differentiated BeWo cells had lesser expression of FABP3 protein than in the undifferentiated cells as the cellular differentiation state was measured by hCG production. In preeclamptic placental tissue, lowered expression of FABP3 protein was observed compared with those in normal pregnancy. All these data indicate that FABP3 may in be part involved in ARA uptake in these cells and its expression may be regulated by ARA, insulin, LXR and the state of cellular differentiation., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Background: Heart type fatty acid protein (HFABP) is a cytosolic protein released early after acute coronary syndrome (ACS) even in the absence of myocardial necrosis., Objectives: The purpose of this systematic review was to determine whether HFABP levels in patients with suspected, or confirmed ACS, improve risk stratification when added to established means of risk assessment., Methods: We searched Medline, Pubmed and Embase databases from inception to July 2015 to identify prospective studies with suspected or confirmed ACS, who had HFABP measured during the index admission with at least 1 month follow up data. A prognostic event was defined as allcause mortality or acute myocardial infarction (AMI)., Results: 7 trials providing data on 6935 patients fulfilled inclusion criteria. There were considerable differences between studies and this was manifest in variation in prognostic impact of elevated HFABP(Odds ratio range 1.2-15.2 for death). All studies demonstrated that HFABP provide unadjusted prognostic information and in only one study this was negated after adjusting for covariates. A combination of both negative troponin and normal HFABP conferred a very low event rate. No study evaluated the incremental value of HFABP beyond that of standard risk scores. Only one study used a high sensitive troponin assay., Conclusion: There was marked heterogeneity in prognostic impact of HFABP in ACS between studies reflecting differences in sampling times and population risk. Prospective studies of suspected ACS with early sampling of HFABP in the era of high sensitivity troponin are necessary to determine the clinical value of HFABP. HFABP should not currently be used clinically as a prognostic marker in patients with suspected ACS., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)