Mitochondrial Contact Sites in Inflammation-Induced Cardiovascular Disease

Líu, Hao; Liu, Xiao; Zhuang, Haixia; Fan, Haoyu; Zhu, Dongxing; Xu, Yiming; He, Pengcheng; Liu, Jinbao; Feng, Du

doi:10.3389/fcell.2020.00692

Cited by 8 publications

(6 citation statements)

References 145 publications

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“…High blood pressure triggers the NOD-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasome in cardiomyocytes through calcium/calmodulin-dependent protein kinase II-delta (CaMKIId) activation. Consecutively, macrophage activation and infiltration lead to fibrosis, compromising contractility [ 20 ]. Calcium leakage via the ryanodine receptor type 2 (RYR2) mutant channels or the influx provoked by BCL2/adenovirus E1B interacting protein 3 (BNIP3) overexpression contributes to cardiomyocyte apoptosis and, finally, to heart failure [ 21 ].…”

Section: Systemic Inflammatory Cytokines Influence Intracellular Calcium Homeostasis and Myocardial Contractilitymentioning

confidence: 99%

Targeting Mediators of Inflammation in Heart Failure: A Short Synthesis of Experimental and Clinical Results

Szabo

Frigy

Nagy

2021

IJMS

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Inflammation has emerged as an important contributor to heart failure (HF) development and progression. Current research data highlight the diversity of immune cells, proteins, and signaling pathways involved in the pathogenesis and perpetuation of heart failure. Chronic inflammation is a major cardiovascular risk factor. Proinflammatory signaling molecules in HF initiate vicious cycles altering mitochondrial function and perturbing calcium homeostasis, therefore affecting myocardial contractility. Specific anti-inflammatory treatment represents a novel approach to prevent and slow HF progression. This review provides an update on the putative roles of inflammatory mediators involved in heart failure (tumor necrosis factor-alpha; interleukin 1, 6, 17, 18, 33) and currently available biological and non-biological therapy options targeting the aforementioned mediators and signaling pathways. We also highlight new treatment approaches based on the latest clinical and experimental research.

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Section: Systemic Inflammatory Cytokines Influence Intracellular Calcium Homeostasis and Myocardial Contractilitymentioning

confidence: 99%

Targeting Mediators of Inflammation in Heart Failure: A Short Synthesis of Experimental and Clinical Results

Szabo

Frigy

Nagy

2021

IJMS

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“…The intensity of inflammation in NR-Early injury biopsies reminds us of the dynamic relationship between cardiac myocytes and macrophages in health and disease. [65][66][67][68][69][70][71][72][73][74] Cardiac myocytes are notoriously vulnerable to injury and can evoke inflammation. This may involve vesicles released by myocytes reminiscent of neural exophers 75 that contain cardiac mitochondria and their DNA, which can trigger innate immunity.…”

Section: The 4 Archetype Model In 889 Emb Identified Biopsies That We...mentioning

confidence: 99%

The Molecular Microscope Diagnostic System: Assessment of Rejection and Injury in Heart Transplant Biopsies

Halloran

Madill‐Thomsen

2022

Transplantation

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This review describes the development of the Molecular Microscope Diagnostic System (MMDx) for heart transplant endomyocardial biopsies (EMBs). MMDx-Heart uses microarrays to measure biopsy-based gene expression and ensembles of machine learning algorithms to interpret the results and compare each new biopsy to a large reference set of earlier biopsies. MMDx assesses T cell–mediated rejection (TCMR), antibody-mediated rejection (AMR), recent parenchymal injury, and atrophy-fibrosis, continually “learning” from new biopsies. Rejection-associated transcripts mapped in kidney transplants and experimental systems were used to identify TCMR, AMR, and recent injury-induced inflammation. Rejection and injury emerged as gradients of intensity, rather than binary classes. AMR was one-third donor-specific antibody (DSA)-negative, and many EMBs first considered to have no rejection displayed minor AMR-like changes, with increased probability of DSA positivity and subtle inflammation. Rejection-associated transcript–based algorithms now classify EMBs as “Normal,” “Minor AMR changes,” “AMR,” “possible AMR,” “TCMR,” “possible TCMR,” and “recent injury.” Additionally, MMDx uses injury-associated transcript sets to assess the degree of parenchymal injury and atrophy-fibrosis in every biopsy and study the effect of rejection on the parenchyma. TCMR directly injures the parenchyma whereas AMR usually induces microcirculation stress but relatively little initial parenchymal damage, although slowly inducing parenchymal atrophy-fibrosis. Function (left ventricular ejection fraction) and short-term risk of failure are strongly determined by parenchymal injury. These discoveries can guide molecular diagnostic applications, either as a central MMDx system or adapted to other platforms. MMDx can also help calibrate noninvasive blood-based biomarkers to avoid unnecessary biopsies and monitor response to therapy.

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“…These cellular activities have crucial roles in several pathologies including but not limited to cardiovascular disease and cancer. Recently, we have extensively reviewed the functional and mechanistic roles of MAMs in inflammation and cardiovascular disease (Liu et al, 2020 ). In the current review, we will highlight the multiple physiological functions of MAMs in mitochondrial Ca 2+ signaling, metabolism and autophagy, and discuss how alterations in MAMs contribute to carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

Mitochondria-Associated Endoplasmic Reticulum Membranes in Breast Cancer

Sun

Gong

et al. 2021

Front. Cell Dev. Biol.

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Mitochondria-associated ER membranes (MAMs) represent a crucial intracellular signaling hub, that regulates various cellular events including Ca2+ homeostasis, lipid metabolism, mitochondrial function, and cellular survival and death. All of these MAM-mediated cellular events contribute to carcinogenesis. Indeed, altered functions of MAMs in several types of cancers have been documented, in particular for breast cancer. Over the past years, altered expression of many MAM-resident proteins have been reported in breast cancer. These MAM-resident proteins play an important role in regulation of breast cancer initiation and progression. In the current review, we discuss our current knowledge about the functions of MAMs, and address the underlying mechanisms through which MAM-resident proteins regulate breast cancer. A fuller understanding of the pathways through which MAMs regulate breast cancer, and identification of breast cancer-specific MAM-resident proteins may help to develop novel therapeutic strategies for breast cancer.

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Mitochondrial Contact Sites in Inflammation-Induced Cardiovascular Disease

Cited by 8 publications

References 145 publications

Targeting Mediators of Inflammation in Heart Failure: A Short Synthesis of Experimental and Clinical Results

Targeting Mediators of Inflammation in Heart Failure: A Short Synthesis of Experimental and Clinical Results

The Molecular Microscope Diagnostic System: Assessment of Rejection and Injury in Heart Transplant Biopsies

Mitochondria-Associated Endoplasmic Reticulum Membranes in Breast Cancer

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