FHL-1 is not involved in pressure overload-induced maladaptive right ventricular remodeling and dysfunction

Veith, Christine; Neghabian, Dariusch; Luitel, Himal; Wilhelm, Jochen; Egemnazarov, Bakytbek; Muntanjohl, Caja; Fischer, Joan G.; Dahal, Bhola K.; Schermuly, Ralph T.; Ghofrani, Hossein Ardeschir; Grimminger, Friedrich; Fink, Ludger; Kwapiszewska, Grażyna; Weißmann, Norbert; Sydykov, Akylbek

doi:10.1007/s00395-019-0767-5

Cited by 18 publications

(20 citation statements)

References 49 publications

(78 reference statements)

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“…Prolonged reperfusion causes significant changes in both cardiomyocytes and coronary microcirculation. Following 3.5 h of reperfusion, myocardium displays a diffused necrosis band blended with hyper-contracted sarcomeres 18 . Post-ischemic myocardium exhibits massive intravascular accumulation of neutrophils.…”

Section: Pathology Of Coronary Microvascular Ecs Damage In MImentioning

confidence: 99%

Coronary microvascular injury in myocardial infarction: perception and knowledge for mitochondrial quality control

et al. 2021

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Endothelial cells (ECs) constitute the innermost layer in all blood vessels to maintain the structural integrity and microcirculation function for coronary microvasculature. Impaired endothelial function is demonstrated in various cardiovascular diseases including myocardial infarction (MI), which is featured by reduced myocardial blood flow as a result of epicardial coronary obstruction, thrombogenesis, and inflammation. In this context, understanding the cellular and molecular mechanisms governing the function of coronary ECs is essential for the early diagnosis and optimal treatment of MI. Although ECs contain relatively fewer mitochondria compared with cardiomyocytes, they function as key sensors of environmental and cellular stress, in the regulation of EC viability, structural integrity and function. Mitochondrial quality control (MQC) machineries respond to a broad array of stress stimuli to regulate fission, fusion, mitophagy and biogenesis in mitochondria. Impaired MQC is a cardinal feature of EC injury and dysfunction. Hence, medications modulating MQC mechanisms are considered as promising novel therapeutic options in MI. Here in this review, we provide updated insights into the key role of MQC mechanisms in coronary ECs and microvascular dysfunction in MI. We also discussed the option of MQC as a novel therapeutic target to delay, reverse or repair coronary microvascular damage in MI. Contemporary available MQC-targeted therapies with potential clinical benefits to alleviate coronary microvascular injury during MI are also summarized.

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Section: Pathology Of Coronary Microvascular Ecs Damage In MImentioning

confidence: 99%

Coronary microvascular injury in myocardial infarction: perception and knowledge for mitochondrial quality control

et al. 2021

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“…Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). Samples were incubated with TRIzol reagent (Invitrogen) to extract total RNA [54]. CRNDE, miR-4262, and ZEB1 cDNA were synthesized using the Allin-One™ cDNA Synthesis Kit (FulenGen, Guangzhou, China) [55].…”

Section: Mitochondrial Membrane Potential (Mmp) Assessmentmentioning

confidence: 99%

Melatonin Attenuates ox‐LDL‐Induced Endothelial Dysfunction by Reducing ER Stress and Inhibiting JNK/Mff Signaling

Xie¹,

Zhong

Guo

et al. 2021

Oxidative Medicine and Cellular Longevity

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Endothelial dysfunction, which is characterized by damage to the endoplasmic reticulum (ER) and mitochondria, is involved in a variety of cardiovascular disorders. Here, we explored whether mitochondrial damage and ER stress are associated with endothelial dysfunction. We also examined whether and how melatonin protects against oxidized low-density lipoprotein- (ox-LDL-) induced damage in endothelial cells. We found that CHOP, GRP78, and PERK expressions, which are indicative of ER stress, increased significantly in response to ox-LDL treatment. ox-LDL also induced mitochondrial dysfunction as evidenced by decreased mitochondrial membrane potential, increased mitochondrial ROS levels, and downregulation of mitochondrial protective factors. In addition, ox-LDL inhibited antioxidative processes, as evidenced by decreased antioxidative enzyme activity and reduced Nrf2/HO-1 expression. Melatonin clearly reduced ER stress and promoted mitochondrial function and antioxidative processes in the presence of ox-LDL. Molecular investigation revealed that ox-LDL activated the JNK/Mff signaling pathway, and melatonin blocked this effect. These results demonstrate that ox-LDL induces ER stress and mitochondrial dysfunction and activates the JNK/Mff signaling pathway, thereby contributing to endothelial dysfunction. Moreover, melatonin inhibited JNK/Mff signaling and sustained ER homeostasis and mitochondrial function, thereby protecting endothelial cells against ox-LDL-induced damage.

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“…Previous studies have shown that ER stress and oxidative stress were extremely significant in macrophage polarization and proinflammatory factor secretion [ 58 – 60 ]. ER stress, oxidative stress, and inflammatory response together make up defense networks of the cells that react to outside stimuli [ 8 , 61 ].…”

Section: Discussionmentioning

confidence: 99%

BTK Promotes Atherosclerosis by Regulating Oxidative Stress, Mitochondrial Injury, and ER Stress of Macrophages

Qiu

Chen

et al. 2021

Oxidative Medicine and Cellular Longevity

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Atherosclerosis (AS) is a chronic metabolic disease in arterial walls, characterized by lipid deposition and persistent aseptic inflammation. AS is regarded as the basis of a variety of cardiovascular and cerebrovascular diseases. It is widely acknowledged that macrophages would become foam cells after internalizing lipoprotein particles, which is an initial factor in atherogenesis. Here, we showed the influences of Bruton’s tyrosine kinase (BTK) in macrophage-mediated AS and how BTK regulates the inflammatory responses of macrophages in AS. Our bioinformatic results suggested that BTK was a potential hub gene, which is closely related to oxidative stress, ER stress, and inflammation in macrophage-induced AS. Moreover, we found that BTK knockdown could restrain ox-LDL-induced NK-κB signaling activation in macrophages and repressed M1 polarization. The mechanistic studies revealed that oxidative stress, mitochondrial injury, and ER stress in macrophages were also suppressed by BTK knockdown. Furthermore, we found that sh-BTK adenovirus injection could alleviate the severity of AS in ApoE-/- mice induced by a high-fat diet in vivo. Our study suggested that BTK promoted ox-LDL-induced ER stress, oxidative stress, and inflammatory responses in macrophages, and it may be a potential therapeutic target in AS.

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FHL-1 is not involved in pressure overload-induced maladaptive right ventricular remodeling and dysfunction

Cited by 18 publications

References 49 publications

Coronary microvascular injury in myocardial infarction: perception and knowledge for mitochondrial quality control

Coronary microvascular injury in myocardial infarction: perception and knowledge for mitochondrial quality control

Melatonin Attenuates ox‐LDL‐Induced Endothelial Dysfunction by Reducing ER Stress and Inhibiting JNK/Mff Signaling

BTK Promotes Atherosclerosis by Regulating Oxidative Stress, Mitochondrial Injury, and ER Stress of Macrophages

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