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Adipose tissue (AT) is a highly heterogeneous organ. Beside the heterogeneity associated to different tissue types (white, brown, and 'brite') and its location-related heterogeneity (subcutaneous, visceral, epicardial, and perivascular, etc.), AT composition, structure, and functionality are highly dependent on individual-associated factors. As such, the pro-inflammatory state associated to the presence of obesity and other cardiovascular risk factors (CVRFs) directly affects AT metabolism. Furthermore, the adipose-derived stem cells (ASCs) that reside in the stromal vascular fraction of AT, besides being responsible for most of the plasticity attributed to AT, is an additional source of heterogeneity. Thus, ASCs directly contribute to AT homeostasis, cell renewal, and spontaneous repair. These ASCs share many properties with the bone-marrow mesenchymal stem cells (i.e. potential to differentiate towards multiple tissue lineages, and angiogenic, antiapoptotic, and immunomodulatory properties). Moreover, ASCs show clear advantages in terms of accessibility and quantity of available sample, their easy in vitro expansion, and the possibility of having an autologous source. All these properties point out towards a potential use of ASCs in regenerative medicine. However, the presence of obesity and other CVRFs induces a pro-inflammatory state that directly impacts ASCs proliferation and differentiation capacities affecting their regenerative abilities. The focus of this review is to summarize how inflammation affects the different AT depots and the mechanisms by which these changes further enhance the obesity-associated metabolic disturbances. Furthermore, we highlight the impact of obesity-induced inflammation on ASCs properties and how those effects impair their plasticity.

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Acute myocardial infarction (AMI) is one of the major causes of mortality and morbidity worldwide. Despite all the efforts, there is a lack of early markers for prevention, diagnosis, and treatment of ischemic syndromes. By applying a proteomic expression profiling approach to identify biomarkers of early stages of AMI, we have detected significant changes in Apolipoprotein J/clusterin (ApoJ) in patients with an acute new-onset myocardial infarction. ApoJ characterization by bidimensional electrophoresis (2-DE), followed by mass spectrometry (MALDI-TOF) depicted a cluster of 13 spots (pI, 4.5-5.0; M(w), 37.1-47.3 kDa) with a significantly different distribution between AMI-patients and controls. Specifically, spots 2, 3, 7, 10, and 13 showed a 2-fold increase in their intensity in AMI-patients (P = 0.001). Western-blot analysis (WB) for total serum ApoJ depicted two bands of 40-45 and 65-70 kDa. When only glycosylated forms were analyzed, the band of 65-70 kDa was the most predominant one. A 25% decrease (P = 0.05) of ApoJ glycosylated forms in AMI-patients was detected by 2-DE. Serum ApoJ levels, determined by a commercial ELISA, were significantly lower (P < 0.001) in AMI-patients (n = 39) immediately after the event than in controls (n = 60). In 60% of patients, the lowest ApoJ level was detected within 6 h after the onset of AMI. Between 72 and 96 h after admission, ApoJ values in AMI-patients had reached control levels. Our results demonstrate alterations in ApoJ proteomic profile, due to a differential glycosylation pattern, in AMI-patients within the first 6 h after the onset of the event. Therefore, the analysis of this isoform glycosylation shift in patients with AMI may be of better use to understand ApoJ function than the total serum levels of ApoJ and this isoform shift may become an early marker of AMI.

Coronary thrombi show rapid dynamic changes both in structure and cell composition as a function of elapsed onset-of-pain-to-PCI time. Aged ischaemic thrombi were more likely to have reduced Pfn-1 content releasing Pfn-1 to the circulation. Onset-of-pain-to-PCI elapsed time in STEMI patients and hence age of occlusive thrombus can be profiled by Pfn-1 levels found in the peripheral circulation.

We demonstrate that hypercholesterolemia induces HDL lipidomic changes, losing phosphatidylcholine-lipid species and gaining cholesteryl esters, and proteomic changes, with losses in cardioprotective proteins. These remodeling changes shifted HDL particles toward a dysfunctional state.

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