Fat cells and membranous fat necrosis of aortic valves: A clinicopathological study

Matsukuma, Susumu; Takeo, Hiroaki; Kono, Takako; Sato, Kimiya

doi:10.1111/pin.12074

Cited by 8 publications

(15 citation statements)

References 19 publications

(39 reference statements)

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“…Recent studies [18] demonstrated that fat cells located mainly in the spongiosa layer can be found in the majority of aortic valve cusps, both in dysfunctional and non-dysfunctional valves. For subcutaneous adipocytes it is known that they actively influence metabolic indices and secrete signaling molecules, including those that affect the parameters also relevant for the physiology of the heart [14,33].…”

Section: Resultsmentioning

confidence: 99%

Heart valve stenosis in laser spotlights: Insights into a complex disease

Büttner

Galli

Jannasch

et al. 2014

Clinical Hemorheology and Microcirculation

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Degenerative heart valve disease is a life-threatening disease affecting about 3% of the population over 65 years. Up to date, cardiac surgery with heart valve replacement is the only available therapy. The disease is characterized by degenerative disorganization of the heart valve structure and alterations in the residing cell populations. Causes and mechanisms of disease genesis are still not fully understood and until now pharmacological therapies are not available. Thus there is enormous interest in new technologies that enable a better characterization of structure and composition of diseased valves. Currently most research techniques demand for extensive processing of extracted valve material. We present a novel approach combining coherent anti-Stokes Raman scattering, endogenous two-photon excited fluorescence and second harmonic generation. Cusp constituents can be examined simultaneously, three-dimensionally and without extensive manipulation of the sample enabling impressive insights into a complex disease.

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Section: Resultsmentioning

confidence: 99%

Heart valve stenosis in laser spotlights: Insights into a complex disease

Büttner

Galli

Jannasch

et al. 2014

Clinical Hemorheology and Microcirculation

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“…Some authors have designated LFN as membranes with an 'arabesque' (7)(8)(9)11,16,33) or 'frost on a windowpane' (34) appearance. LFN is scattered singly or in some clusters within fatty and/or fibrous tissues and shows microcystic, macrocystic, and/or crushed features (7)(8)(9)(10)(11)(12)(14)(15)(16)19,(21)(22)(23)(24)(25)(26)28). Scattered LFN within fatty tissues represents early changes of LFN, and LFN within fibrous tissues may represent chronic phase lesions (9,12,(14)(15)(16)18,19,21,35).…”

Section: Morphological Characteristics Of Lfnmentioning

confidence: 99%

“…LFN is also highlighted by periodic acid-Schiff staining with or without diastase digestion (Fig. 1C) (7)(8)(9)(10)(11)(12)16,18,(22)(23)(24)(25)(26)(28)(29)(30)35), Sudan black B staining (10,11,16,22,(24)(25)(26)(27)30,31), oil red O staining (23), orcein staining (10), long Ziehl-Neelsen staining (16,(23)(24)(25)(26)(27), silver impregnation (30,31), phosphotungstic acid-hematoxylin staining (11,16), and luxol fast blue staining (11,16,22,23,27,30,31). LFN occasionally shows noncystic, crushed features embedded within fibrous tissues and may be difficult to recognize (Fig.…”

Section: Morphological Characteristics Of Lfnmentioning

confidence: 99%

“…Such necrotic fat cells or lipogranulomatous lesions can be resolved during the relatively early stages of the disease. However, another unique form of white fat necrosis, designated lipomembranous fat necrosis (LFN) (7)(8)(9)(10)(11)(12)(13)(14)(15), also called lipomembranous changes (8,(15)(16)(17)(18)(19)(20)(21), membranous fat necrosis (1,15,(22)(23)(24)(25)(26)(27)(28)(29), membranocystic changes or fat necrosis (7,8,11,(14)(15)(16)(17)(28)(29)(30)(31)(32)(33)(34), membranous lipodystrophy-like changes (30,31), and pseudomembranous fat necrosis (7,35), is found in fibrotic tissues or later stages of various diseases (9,12,…”

Section: Introductionmentioning

confidence: 99%

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Lipomembranous fat necrosis: A distinctive and unique morphology (Review)

et al. 2022

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Lipomembranous fat necrosis (LFN) is an uncommon but distinct form of fat necrosis, which is characterized by eosinophilic, crenulated and/or serpiginous membranes. LFN exhibits macrocystic, microcystic and/or crushed features. LFN is routinely detectable on hematoxylin and eosin (H&E)-stained sections, and is present both in the acute phase and in the later or fibrous stage of necrotic fatty lesions. Smaller crushed LFN embedded within fibrous tissues may be difficult to recognize on H&E-stained sections, but can be highlighted by some staining techniques, including Masson trichrome, periodic acid-Schiff, orcein, long Ziehl-Neelsen stain, silver impregnation, phosphotungstic acid-hematoxylin and luxol fast blue staining. LFN was initially considered a specific feature of Nasu-Hakola disease, but has since been identified in various subcutaneous or intraabdominal lesions related to ischemic conditions or venous insufficiency. In addition, LFN is detectable in intra-articular loose bodies and aortic valves with or without dysfunction, suggesting that LFN is also associated with ischemia-like hypoxic conditions or malnutrition. LFN is considered to be a histological hallmark of hidden ischemic or hypoxic/malnourished conditions in various diseases; however, the exact mechanisms of LFN remain poorly understood. The present review described the clinicopathological features of this interesting, but poorly characterized, condition.

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“…Calcific aortic valve stenosis (CAVS) is regarded as a multifactorial disorder, whose pathogenesis includes mechanical stress [1], extracellular matrix remodelling [2], lipid accumulation and/or alteration [3], oxidative stress [4], inflammation [5], a decrease in anti-calcific factors [6], mineral imbalance [7], angiogenesis [8], and heterotopic ossification, depending on osteoblastic transdifferentiation of aortic valve interstitial cells (AVICs) [9]. Except for the unquestionable concept that ossification implies calcification but not vice versa, as matter of fact the most common event preceding and likely triggering all calcific aortic valve diseases is AVIC alteration and/or death in its various forms as reported [10][11][12][13]. In addition to (i) calcium-binding osteopontin (OPN), osteocalcin, and osteonectin [14,15], (ii) proteoglycans rich in acidic glycosaminoglycan lateral chains [16], and (iii) alkaline phosphatase (ALP) [17], increasing attention has been focused on the role of phospholipases (PLAs) in CAVS onset, with a particular focus on circulating lipoprotein-associated PLA isoforms [18,19].…”

Section: Introductionmentioning

confidence: 99%

Calcium-Dependent Cytosolic Phospholipase A2α as Key Factor in Calcification of Subdermally Implanted Aortic Valve Leaflets

Bonetti

Contin

Tonon

et al. 2022

IJMS

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Calcium-dependent cytosolic phospholipase A2α (cPLA2α) had been previously found to be overexpressed by aortic valve interstitial cells (AVICs) subjected to in vitro calcific induction. Here, cPLA2α expression was immunohistochemically assayed in porcine aortic valve leaflets (iAVLs) that had undergone accelerated calcification subsequent to 2- to 28-day-long implantation in rat subcutis. A time-dependent increase in cPLA2α-positive AVICs paralleled mineralization progression depending on dramatic cell membrane degeneration with the release of hydroxyapatite-nucleating acidic lipid material, as revealed by immunogold particles decorating organelle membranes in 2d-iAVLs, as well as membrane-derived lipid byproducts in 7d- to 28d-iAVLs. Additional positivity was detected for (i) pro-inflammatory IL-6, mostly exhibited by rat peri-implant cells surrounding 14d- and 28d-iAVLs; (ii) calcium-binding osteopontin, with time-dependent increase and no ossification occurrence; (iii) anti-calcific fetuin-A, mostly restricted to blood plasma within vessels irrorating the connective envelopes of 28d-iAVLs; (iv) early apoptosis marker annexin-V, limited to sporadic AVICs in all iAVLs. No positivity was found for either apoptosis executioner cleaved caspase-3 or autophagy marker MAP1. In conclusion, cPLA2α appears to be a factor characterizing AVL calcification concurrently with a distinct still uncoded cell death form also in an animal model, as well as a putative target for the prevention and treatment of calcific valve diseases.

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Fat cells and membranous fat necrosis of aortic valves: A clinicopathological study

Cited by 8 publications

References 19 publications

Heart valve stenosis in laser spotlights: Insights into a complex disease

Heart valve stenosis in laser spotlights: Insights into a complex disease

Lipomembranous fat necrosis: A distinctive and unique morphology (Review)

Calcium-Dependent Cytosolic Phospholipase A2α as Key Factor in Calcification of Subdermally Implanted Aortic Valve Leaflets

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