Syncytium calcium signaling and macrophage function in the heart

Zhou, Xin; Li, Zhong-Guang; Wang, Zefan; Chen, Eda; Wang, Juan; Chen, Frederic; Jones, Odell; Tan, Tao; Chen, Shawn; Takeshima, Hiroshi; Bryant, Joseph; Ma, Jianjie; Xu, Xuehong

doi:10.1186/s13578-018-0222-6

Cited by 12 publications

(9 citation statements)

References 55 publications

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“…One recent study suggested that TRPV2, as well as the TRP superfamily M2 (TRPM2) may be involved in this myocyte-macrophage interaction at the intercalated disk, by a mechanism that is yet to be investigated. It is postulated that this chain of events enables the formation of a connecting structure between macrophages and cardiomyocytes, along with the extracellular matrix, which guarantees synchronization of cardiomyocyte contraction (78).…”

Section: Trpv2-expressing Resident Cardiac Macrophagesmentioning

confidence: 99%

Potential roles in cardiac physiology and pathology of the cation channel TRPV2 expressed in cardiac cells and cardiac macrophages: a mini-review

Entin–Meer

Keren

2020

American Journal of Physiology-Heart and Circulatory Physiology

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TRPV2 is a well-conserved channel protein expressed in almost all tissues. Cardiomyocyte TRPV2 is expressed in the intercalated disks of the cardiac sarcomeres, where it is involved in maintaining the proper mechanoelectric coupling and structure. It is also abundantly expressed in the intracellular pools, mainly the endoplasmic reticulum. Under pathological conditions, TRPV2 is translocated to the sarcolemma, where it mediates an abnormal [Ca]2+ entry that may contribute to disease progression. In addition, an intracellularly diffused TRPV2 expression is present in resident cardiac macrophages. Upon infection or inflammation, TRPV2 is engaged in early phagosomes and is, therefore, potentially involved in protecting the cardiac tissue. Following acute myocardial infarction, a profound elevated expression of TRPV2 is observed on the cell membrane of the peri-infarct macrophages. The macrophage TRPV2 may harbor a detrimental effect in cardiac recovery by increasing unfavorable migration and phagocytosis processes in the injured heart. Most reports suggest that while cardiac TRPV2 activation may be beneficial under specific physiological conditions, both cardiac- and macrophage-related TRPV2 blocking can significantly ameliorate disease progression in various pathological states. To verify this possibility, the time frame of TRPV2 overexpression and its mediated signaling need to be fully characterized in both cardiomyocyte and cardiac macrophage populations.

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Section: Trpv2-expressing Resident Cardiac Macrophagesmentioning

confidence: 99%

Potential roles in cardiac physiology and pathology of the cation channel TRPV2 expressed in cardiac cells and cardiac macrophages: a mini-review

Entin–Meer

Keren

2020

American Journal of Physiology-Heart and Circulatory Physiology

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“…In both tumorigenesis and cardiovascular pathology, calcium (Ca 2+ ) is considerate to be an essential constituent vital to the healthy physiology and disease pathology of both tumor cells and myocytes [21][22][23][24]. In regulation of cellular proliferation and apoptotic death, AKT/ AMPK pathway control the cell cycle by targeting on critical point of G2/S transition functioning along with Ras and Cyclin D1.…”

Section: Introductionmentioning

confidence: 99%

Multiple functions of autophagy in vascular calcification

Zhou

Yuan

et al. 2021

Cell Biosci

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Background Vascular calcification is a closely linked to cardiovascular diseases, such as atherosclerosis, chronic kidney disease, diabetes, hypertension and aging. The extent of vascular calcification is closely correlate with adverse clinical events and cardiovascular all-cause mortality. The role of autophagy in vascular calcification is complex with many mechanistic unknowns. Methods In this review, we analyze the current known mechanisms of autophagy in vascular calcification and discuss the theoretical advantages of targeting autophagy as an intervention against vascular calcification. Results Here we summarize the functional link between vascular calcification and autophagy in both animal models of and human cardiovascular disease. Firstly, autophagy can reduce calcification by inhibiting the osteogenic differentiation of VSMCs related to ANCR, ERα, β-catenin, HIF-1a/PDK4, p62, miR-30b, BECN1, mTOR, SOX9, GHSR/ERK, and AMPK signaling. Conversely, autophagy can induce osteoblast differentiation and calcification as mediated by CREB, degradation of elastin, and lncRNA H19 and DUSP5 mediated ERK signaling. Secondly, autophagy also links apoptosis and vascular calcification through AMPK/mTOR/ULK1, Wnt/β-catenin and GAS6/AXL synthesis, as apoptotic cells become the nidus for calcium-phosphate crystal deposition. The failure of mitophagy can activate Drp1, BNIP3, and NR4A1/DNA‑PKcs/p53 mediated intrinsic apoptotic pathways, which have been closely linked to the formation of vascular calcification. Additionally, autophagy also plays a role in osteogenesis by regulating vascular calcification, which in turn regulates expression of proteins related to bone development, such as osteocalcin, osteonectin, etc. and regulated by mTOR, EphrinB2 and RhoA. Furthermore, autophagy also promotes vitamin K2-induced MC3T3 E1 osteoblast differentiation and FGFR4/FGF18- and JNK/complex VPS34–beclin-1-related bone mineralization via vascular calcification. Conclusion The interaction between autophagy and vascular calcification are complicated, with their interaction affected by the disease process, anatomical location, and the surrounding microenvironment. Autophagy activation in existent cellular damage is considered protective, while defective autophagy in normal cells result in apoptotic activation. Identifying and maintaining cells at the delicate line between these two states may hold the key to reducing vascular calcification, in which autophagy associated clinical strategy could be developed.

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“…As the most complicated issue, physiological function and disorder of heart are determined by multiple factors including EC coupling pathway in cardiomyocytes [82], voltage-dependent gate and connexins pathway in cardiac conduction system [83], macrophage associated regulation of cardiac conduction [82,84], and nutrient delivery involved epithelial vascular system. It is rational to believe that the molecular mechanism of long-term MICT exercise on improvement and protection of cardiac function should be involved in the most pathways related to daily cardiac physiology.…”

Section: Classification Of Long-term Exercise Models and Exercise-indmentioning

confidence: 99%

A systematic comparison of exercise training protocols on animal models of cardiovascular capacity

Feng

Wang

et al. 2019

Life Sciences

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Cardiovascular disease (CVD) is a major global cause of mortality, which has prompted numerous studies seeking to reduce the risk of heart failure and sudden cardiac death. While regular physical activity is known to improve CVD associated morbidity and mortality, the optimal duration, frequency, and intensity of exercise remains unclear. To address this uncertainty, various animal models have been used to study the cardioprotective effects of exercise and related molecular mechanism such as the mice training models significantly decrease size of myocardial infarct by affecting Kir6.1, VSMC sarc-KATP channels, and pulmonary eNOS. Although these findings cement the importance of animal models in studying exercise induced cardioprotection, the vast assortment of exercise protocols makes comparison across studies difficult. To address this issue, we review and break down the existent exercise models into categories based on exercise modality, intensity, frequency, and duration. The timing of sample collection is also compared and sorted into four distinct phases: pre-exercise (Phase I), mid-exercise (Phase II), exercise recovery (Phase III), and post-exercise (Phase IV). Finally, because the life-span of animals so are limited, small changes in animal exercise duration can corresponded to untenable amounts of human exercise. To address this limitation, we introduce the Life-Span Relative Exercise Time (RETlife span) as a method of accurately defining short-term, medium-term and long-term exercise relative to the animal’s life expectancy. Systematic organization of existent protocols and this new system of defining exercise duration will allow for a more solid framework from which researchers can extrapolate animal model data to clinical application.

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Syncytium calcium signaling and macrophage function in the heart

Cited by 12 publications

References 55 publications

Potential roles in cardiac physiology and pathology of the cation channel TRPV2 expressed in cardiac cells and cardiac macrophages: a mini-review

Potential roles in cardiac physiology and pathology of the cation channel TRPV2 expressed in cardiac cells and cardiac macrophages: a mini-review

Multiple functions of autophagy in vascular calcification

A systematic comparison of exercise training protocols on animal models of cardiovascular capacity

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