Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Cardiac immune cell infiltration associates with abnormal lipid metabolism

V. Cifarelli, O. Kuda, K. Yang, X. Liu, RW. Gross, TA. Pietka, GS. Heo, D. Sultan, H. Luehmann, J. Lesser, M. Ross, IJ. Goldberg, RJ. Gropler, Y. Liu, NA. Abumrad

. 2022 ; 9 (-) : 948332. [pub] 20220817

Jazyk angličtina Země Švýcarsko

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc22023506

Grantová podpora
R01 HL045095 NHLBI NIH HHS - United States

CD36 mediates the uptake of long-chain fatty acids (FAs), a major energy substrate for the myocardium. Under excessive FA supply, CD36 can cause cardiac lipid accumulation and inflammation while its deletion reduces heart FA uptake and lipid content and increases glucose utilization. As a result, CD36 was proposed as a therapeutic target for obesity-associated heart disease. However, more recent reports have shown that CD36 deficiency suppresses myocardial flexibility in fuel preference between glucose and FAs, impairing tissue energy balance, while CD36 absence in tissue macrophages reduces efferocytosis and myocardial repair after injury. In line with the latter homeostatic functions, we had previously reported that CD36-/- mice have chronic subclinical inflammation. Lipids are important for the maintenance of tissue homeostasis and there is limited information on heart lipid metabolism in CD36 deficiency. Here, we document in the hearts of unchallenged CD36-/- mice abnormalities in the metabolism of triglycerides, plasmalogens, cardiolipins, acylcarnitines, and arachidonic acid, and the altered remodeling of these lipids in response to an overnight fast. The hearts were examined for evidence of inflammation by monitoring the presence of neutrophils and pro-inflammatory monocytes/macrophages using the respective positron emission tomography (PET) tracers, 64Cu-AMD3100 and 68Ga-DOTA-ECL1i. We detected significant immune cell infiltration in unchallenged CD36-/- hearts as compared with controls and immune infiltration was also observed in hearts of mice with cardiomyocyte-specific CD36 deficiency. Together, the data show that the CD36-/- heart is in a non-homeostatic state that could compromise its stress response. Non-invasive immune cell monitoring in humans with partial or total CD36 deficiency could help evaluate the risk of impaired heart remodeling and disease.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc22023506
003      
CZ-PrNML
005      
20221031095218.0
007      
ta
008      
221010s2022 sz f 000 0|eng||
009      
AR
024    7_
$a 10.3389/fcvm.2022.948332 $2 doi
035    __
$a (PubMed)36061565
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a sz
100    1_
$a Cifarelli, Vincenza $u Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States $u Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO, United States
245    10
$a Cardiac immune cell infiltration associates with abnormal lipid metabolism / $c V. Cifarelli, O. Kuda, K. Yang, X. Liu, RW. Gross, TA. Pietka, GS. Heo, D. Sultan, H. Luehmann, J. Lesser, M. Ross, IJ. Goldberg, RJ. Gropler, Y. Liu, NA. Abumrad
520    9_
$a CD36 mediates the uptake of long-chain fatty acids (FAs), a major energy substrate for the myocardium. Under excessive FA supply, CD36 can cause cardiac lipid accumulation and inflammation while its deletion reduces heart FA uptake and lipid content and increases glucose utilization. As a result, CD36 was proposed as a therapeutic target for obesity-associated heart disease. However, more recent reports have shown that CD36 deficiency suppresses myocardial flexibility in fuel preference between glucose and FAs, impairing tissue energy balance, while CD36 absence in tissue macrophages reduces efferocytosis and myocardial repair after injury. In line with the latter homeostatic functions, we had previously reported that CD36-/- mice have chronic subclinical inflammation. Lipids are important for the maintenance of tissue homeostasis and there is limited information on heart lipid metabolism in CD36 deficiency. Here, we document in the hearts of unchallenged CD36-/- mice abnormalities in the metabolism of triglycerides, plasmalogens, cardiolipins, acylcarnitines, and arachidonic acid, and the altered remodeling of these lipids in response to an overnight fast. The hearts were examined for evidence of inflammation by monitoring the presence of neutrophils and pro-inflammatory monocytes/macrophages using the respective positron emission tomography (PET) tracers, 64Cu-AMD3100 and 68Ga-DOTA-ECL1i. We detected significant immune cell infiltration in unchallenged CD36-/- hearts as compared with controls and immune infiltration was also observed in hearts of mice with cardiomyocyte-specific CD36 deficiency. Together, the data show that the CD36-/- heart is in a non-homeostatic state that could compromise its stress response. Non-invasive immune cell monitoring in humans with partial or total CD36 deficiency could help evaluate the risk of impaired heart remodeling and disease.
655    _2
$a časopisecké články $7 D016428
700    1_
$a Kuda, Ondrej $u Institute of Physiology, Czech Academy of Sciences, Prague, Czechia
700    1_
$a Yang, Kui $u Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States $u Division of Complex Drug Analysis, Office of Testing and Research, U.S. Food and Drug Administration, St. Louis, MO, United States
700    1_
$a Liu, Xinping $u Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States
700    1_
$a Gross, Richard W $u Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States
700    1_
$a Pietka, Terri A $u Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States
700    1_
$a Heo, Gyu Seong $u Department of Radiology, Washington University School of Medicine, St. Louis, MO, United States
700    1_
$a Sultan, Deborah $u Department of Radiology, Washington University School of Medicine, St. Louis, MO, United States
700    1_
$a Luehmann, Hannah $u Department of Radiology, Washington University School of Medicine, St. Louis, MO, United States
700    1_
$a Lesser, Josie $u Department of Radiology, Washington University School of Medicine, St. Louis, MO, United States
700    1_
$a Ross, Morgan $u Department of Pharmacology and Physiology, Saint Louis University School of Medicine, St. Louis, MO, United States
700    1_
$a Goldberg, Ira J $u Division of Endocrinology, Department of Medicine, New York University Grossman School of Medicine, New York, NY, United States
700    1_
$a Gropler, Robert J $u Department of Radiology, Washington University School of Medicine, St. Louis, MO, United States
700    1_
$a Liu, Yongjian $u Department of Radiology, Washington University School of Medicine, St. Louis, MO, United States
700    1_
$a Abumrad, Nada A $u Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States $u Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO, United States
773    0_
$w MED00198704 $t Frontiers in cardiovascular medicine $x 2297-055X $g Roč. 9, č. - (2022), s. 948332
856    41
$u https://pubmed.ncbi.nlm.nih.gov/36061565 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y - $z 0
990    __
$a 20221010 $b ABA008
991    __
$a 20221031095216 $b ABA008
999    __
$a ind $b bmc $g 1853890 $s 1174794
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2022 $b 9 $c - $d 948332 $e 20220817 $i 2297-055X $m Frontiers in cardiovascular medicine $n Front Cardiovasc Med $x MED00198704
GRA    __
$a R01 HL045095 $p NHLBI NIH HHS $2 United States
LZP    __
$a Pubmed-20221010

Najít záznam

Citační ukazatele

Možnosti archivace