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Mini Reviews in Medicinal Chemistry 2015MicroRNAs (miRNAs) are a novel class of endogenous, short, non-coding, posttranscriptional RNAs, which play important roles in regulating lots of important biological... (Review)
Review
MicroRNAs (miRNAs) are a novel class of endogenous, short, non-coding, posttranscriptional RNAs, which play important roles in regulating lots of important biological functions. Evidences show that altered expression of miRNAs are involved in pathological hypertrophy and cardiac failure, making it possible to target miRNAs as a novel therapy. In this review, we focus on very recent progresses in the regulation of miRNAs in pathological hypertrophy and cardiac failure. In addition, we also discuss the potential of using miRNAs as a new therapy for pathological hypertrophy and cardiac failure.
Topics: Animals; Heart Failure; Humans; Hypertrophy; MicroRNAs; Molecular Targeted Therapy; Myocardium
PubMed: 25807942
DOI: 10.2174/1389557515666150324124751 -
Immunologic Research Feb 2017Hypertrophic pachymeningitis (HP) is a rare disorder that causes thickening of the dura mater. Inflammatory lesions may be located in the cerebral or spinal dura mater... (Review)
Review
Hypertrophic pachymeningitis (HP) is a rare disorder that causes thickening of the dura mater. Inflammatory lesions may be located in the cerebral or spinal dura mater or, less frequently, in both locations simultaneously. Numerous clinico-pathological entities cause thickening of the pachymeninges. Indeed, HP is a potential manifestation of many different diseases, but the diagnosis often remains uncertain. Cases in which the pachymeningitis has no known aetiology are termed "idiopathic" HP (IHP). Recently, it has been suggested that IgG4-related disease represents a subset of cases previously diagnosed as idiopathic hypertrophic pachymeningitis. Little is known regarding the pathogenic events of IHP. In a general theory, the inflammatory infiltrate, mainly consisting of B and T lymphocytes, activates fibroblasts and induces collagen deposition, leading to tissue hypertrophy and increased dural thickness. Clinical manifestations of IHP depend upon the location of the inflammatory lesions and compression of the adjacent nervous structures. Three central pathological features are lymphoplasmacytic infiltration, obliterative phlebitis, and storiform fibrosis. MRI is the examination of choice for the preliminary diagnosis of IHP. Histopathological examination of a biopsy specimen of the dura mater would finally confirm the diagnosis. The differential diagnosis for HP is broad and includes infections, autoimmune disorders, and neoplasia. Currently, there is no consensus about treatment for patients with IHP. There is a preference for glucocorticoid treatment on diagnosis followed by the addition of other immunosuppressive agents in the event of a recurrence. Rituximab is used in patients who did not respond to glucocorticoids or to conventional steroid-sparing agents.
Topics: Autoimmune Diseases; Diagnosis, Differential; Humans; Hypertrophy; Immunoglobulin G; Meninges; Meningitis; Prognosis
PubMed: 27592235
DOI: 10.1007/s12026-016-8863-1 -
Archives of Biochemistry and Biophysics Oct 2023Maladaptive right ventricular (RV) remodeling is the most important pathological feature of pulmonary hypertension (PH), involving processes such as myocardial...
BACKGROUND
Maladaptive right ventricular (RV) remodeling is the most important pathological feature of pulmonary hypertension (PH), involving processes such as myocardial hypertrophy and fibrosis. A growing number of studies have shown that mitochondria-associated endoplasmic reticulum membranes (MAMs) are involved in various physiological and pathological processes, such as calcium homeostasis, lipid metabolism, inflammatory response, mitochondrial dynamics, and autophagy/mitophagy. The abnormal expression of MAMs-related factors is closely related to the occurrence and development of heart-related diseases. However, the role of MAM-related factors in the maladaptive RV remodeling of PH rats remains unclear.
METHODS AND RESULTS
We first obtained the transcriptome data of RV tissues from PH rats induced by Su5416 combined with hypoxia treatment (SuHx) from the Gene Expression Omnibus (GEO) database. The results showed that two MAMs-related genes (Opa1 and Mfn2) were significantly down-regulated in RV tissues of SuHx rats, accompanied by significant up-regulation of cardiac hypertrophy-related genes (such as Nppb and Myh7). Subsequently, using the SuHx-induced PH rat model, we found that the downregulation of mitochondrial fusion proteins Opa1 and Mfn2 may be involved in maladaptive RV remodeling by accelerating mitochondrial dysfunction. Finally, at the cellular level, we found that overexpression of Opa1 and Mfn2 could inhibit hypoxia-induced mitochondrial fission and reduce ROS production in H9c2 cardiomyocytes, thereby retarded the progression of cardiomyocyte hypertrophy.
CONCLUSIONS
The down-regulation of mitochondrial fusion protein Opa1/Mfn2 can accelerate cardiomyocyte hypertrophy and then participate in maladaptive RV remodeling in SuHx-induced PH rats, which may be potential targets for preventing maladaptive RV remodeling.
Topics: Rats; Animals; Hypertension, Pulmonary; Myocytes, Cardiac; Mitochondrial Dynamics; Down-Regulation; Mitochondrial Proteins; Mitochondria; Hydrolases; Hypoxia; Hypertrophy; Ventricular Remodeling; GTP Phosphohydrolases
PubMed: 37696382
DOI: 10.1016/j.abb.2023.109743 -
Current Opinion in Clinical Nutrition... Jul 2023Heart failure is one of the major causes of death worldwide and continues to increase despite therapeutics and pharmacology advances. Fatty acids and glucose are used as... (Review)
Review
PURPOSE OF REVIEW
Heart failure is one of the major causes of death worldwide and continues to increase despite therapeutics and pharmacology advances. Fatty acids and glucose are used as ATP-producing fuels in heart to meet its energy demands. However, dysregulation of metabolites' use plays a pivotal role in cardiac diseases. How glucose becomes toxic or drives cardiac dysfunction is incompletely understood. In the present review, we summarize the recent findings on cardiac cellular and molecular events that are driven by glucose during pathologic conditions and potential therapeutic strategies to tackle hyperglycemia-mediated cardiac dysfunction.
RECENT FINDINGS
Several studies have emerged recently, demonstrating that excessive glucose utilization has been correlated with impairment of cellular metabolic homeostasis primarily driven by mitochondrial dysfunction and damage, oxidative stress, and abnormal redox signaling. This disturbance is associated with cardiac remodeling, hypertrophy, and systolic and diastolic dysfunction. Both human and animal heart failure studies, report that glucose is a preferable fuel at the expense of fatty acid oxidation during ischemia and hypertrophy, but the opposite happens in diabetic hearts, which warrants further investigation.
SUMMARY
A better understanding of glucose metabolism and its fate during distinct types of heart disease will contribute to developing novel therapeutic options for the prevention and treatment of heart failure.
Topics: Animals; Humans; Glucose; Energy Metabolism; Myocardium; Oxidation-Reduction; Heart Failure; Fatty Acids; Hypertrophy
PubMed: 37144457
DOI: 10.1097/MCO.0000000000000943 -
Circulation Journal : Official Journal... 2016Left ventricular hypertrophy (LVH) is growth in left ventricular mass caused by increased cardiomyocyte size. LVH can be a physiological adaptation to strenuous physical... (Review)
Review
Left ventricular hypertrophy (LVH) is growth in left ventricular mass caused by increased cardiomyocyte size. LVH can be a physiological adaptation to strenuous physical exercise, as in athletes, or it can be a pathological condition, which is either genetic or secondary to LV overload. Physiological LVH is usually benign and regresses upon reduction/cessation of physical activity. Pathological LVH is a compensatory phenomenon, which eventually may become maladaptive and evolve towards progressive LV dysfunction and heart failure (HF). Both interstitial and replacement fibrosis play a major role in the progressive decompensation of the hypertrophied LV. Coronary microvascular dysfunction (CMD) and myocardial ischemia, which have been demonstrated in most forms of pathological LVH, have an important pathogenetic role in the formation of replacement fibrosis and both contribute to the evolution towards LV dysfunction and HF. Noninvasive imaging allows detection of myocardial fibrosis and CMD, thus providing unique information for the stratification of patients with LVH. (Circ J 2016; 80: 555-564).
Topics: Fibrosis; Heart Failure; Humans; Hypertrophy, Left Ventricular; Ventricular Dysfunction, Left
PubMed: 26853555
DOI: 10.1253/circj.CJ-16-0062 -
Clinics in Plastic Surgery Apr 2016Recurrent or persistent macromastia can occur after breast reduction. This may be due to inadequate primary volume reduction, poor postoperative shape, and breast or... (Review)
Review
Recurrent or persistent macromastia can occur after breast reduction. This may be due to inadequate primary volume reduction, poor postoperative shape, and breast or nipple-areola complex asymmetry. Postpartum breast changes, weight change, and aging can also contribute to recurrent macromastia. The concern in these cases is the altered blood supply to the nipple-areola complex and the safety of nipple-areola complex transposition. Literature on the safety of repeated breast reduction is limited with conflicting approaches. This article discusses an approach to recurrent or persistent macromastia and outlines a modified breast reduction technique that is safe in cases of repeated breast reduction.
Topics: Breast; Female; Humans; Hypertrophy; Mammaplasty; Nipples; Recurrence
PubMed: 27012797
DOI: 10.1016/j.cps.2015.12.004 -
American Journal of Physiology. Heart... Sep 2017The energy starvation hypothesis proposes that maladaptive metabolic remodeling antedates, initiates, and maintains adverse contractile dysfunction in heart failure... (Review)
Review
The energy starvation hypothesis proposes that maladaptive metabolic remodeling antedates, initiates, and maintains adverse contractile dysfunction in heart failure (HF). Better understanding of the cardiac metabolic phenotype and metabolic signaling could help identify the role metabolic remodeling plays within HF and the conditions known to transition toward HF, including "pathological" hypertrophy. In this review, we discuss metabolic phenotype and metabolic signaling in the contexts of pathological hypertrophy and HF. We discuss the significance of alterations in energy supply (substrate utilization, oxidative capacity, and phosphotransfer) and energy sensing using observations from human and animal disease models and models of manipulated energy supply/sensing. We aim to provide ways of thinking about metabolic remodeling that center around metabolic flexibility, capacity (reserve), and efficiency rather than around particular substrate preferences or transcriptomic profiles. We show that maladaptive metabolic remodeling takes multiple forms across multiple energy-handling domains. We suggest that lack of metabolic flexibility and reserve (substrate, oxidative, and phosphotransfer) represents a final common denominator ultimately compromising efficiency and contractile reserve in stressful contexts.
Topics: Adaptation, Physiological; Animals; Cardiomegaly; Disease Progression; Energy Metabolism; Heart Failure; Humans; Myocardium; Phenotype
PubMed: 28646030
DOI: 10.1152/ajpheart.00731.2016 -
Endokrynologia Polska 2020Not required for Clinical Vignette.
Not required for Clinical Vignette.
Topics: Breast; Child; Estrogen Antagonists; Female; Humans; Hypertrophy
PubMed: 31909454
DOI: 10.5603/EP.a2019.0063 -
Circulation Research Mar 2023A recent study suggests that systemic hypoxemia in adult male mice can induce cardiac myocytes to proliferate. The goal of the present experiments was to confirm these...
BACKGROUND
A recent study suggests that systemic hypoxemia in adult male mice can induce cardiac myocytes to proliferate. The goal of the present experiments was to confirm these results, provide new insights on the mechanisms that induce adult cardiomyocyte cell cycle reentry, and to determine if hypoxemia also induces cardiomyocyte proliferation in female mice.
METHODS
EdU-containing mini pumps were implanted in 3-month-old, male and female C57BL/6 mice. Mice were placed in a hypoxia chamber, and the oxygen was lowered by 1% every day for 14 days to reach 7% oxygen. The animals remained in 7% oxygen for 2 weeks before terminal studies. Myocyte proliferation was also studied with a mosaic analysis with double markers mouse model.
RESULTS
Hypoxia induced cardiac hypertrophy in both left ventricular (LV) and right ventricular (RV) myocytes, with LV myocytes lengthening and RV myocytes widening and lengthening. Hypoxia induced an increase (0.01±0.01% in normoxia to 0.11±0.09% in hypoxia) in the number of EdU+ RV cardiomyocytes, with no effect on LV myocytes in male C57BL/6 mice. Similar results were observed in female mice. Furthermore, in mosaic analysis with double markers mice, hypoxia induced a significant increase in RV myocyte proliferation (0.03±0.03% in normoxia to 0.32±0.15% in hypoxia of RFP+ myocytes), with no significant change in LV myocyte proliferation. RNA sequencing showed upregulation of mitotic cell cycle genes and a downregulation of Cullin genes, which promote the G1 to S phase transition in hypoxic mice. There was significant proliferation of nonmyocytes and mild cardiac fibrosis in hypoxic mice that did not disrupt cardiac function. Male and female mice exhibited similar gene expression following hypoxia.
CONCLUSIONS
Systemic hypoxia induces a global hypertrophic stress response that was associated with increased RV proliferation, and while LV myocytes did not show increased proliferation, our results minimally confirm previous reports that hypoxia can induce cardiomyocyte cell cycle activity in vivo.
Topics: Mice; Male; Female; Animals; Myocytes, Cardiac; Mice, Inbred C57BL; Hypoxia; Cell Proliferation; Oxygen; Hypertrophy
PubMed: 36799218
DOI: 10.1161/CIRCRESAHA.122.321604 -
BMC Pediatrics Apr 2023When analyzing the relationship between adenotonsillar hypertrophy and craniofacial morphology, researchers generally regarded hypertrophied adenoids and tonsils as a...
BACKGROUND
When analyzing the relationship between adenotonsillar hypertrophy and craniofacial morphology, researchers generally regarded hypertrophied adenoids and tonsils as a whole. It remains unclear whether different enlarged sites of pharyngeal lymphoid tissue would correlate with multiple craniofacial subtypes. We hypothesized there would be craniofacial subtypes correlated with different locations of hypertrophied adenoid and tonsil.
METHODS
Lateral cephalometric radiographs were obtained from 466 children (171 boys and 295 girls, aged 12.27 ± 2.69 years). They were divided into four groups according to different sites of enlarged pharyngeal lymphoid tissue: adenoid hypertrophy group (AG, n = 126), tonsillar hypertrophy group (TG, n = 59), adenotonsillar hypertrophy group (ATG, n = 69) and control group (CG, n = 212). Five commonly used angles for cephalometric measurements were investigated: SNA (Sella-Nasion-Point A), SNB (Sella-Nasion-Point B), ANB (Point A-Nasion-Point B), mandibular plane angle (MP/SN) and Y-axis angle (SGn/FH).
RESULTS
Children with isolated tonsillar hypertrophy correlated with increased SNA (unstandardized regression coefficient B = 1.38, p = 0.009) and SNB (B = 1.99, p = 0.001) compared with controls. However, children with isolated adenoid hypertrophy correlated with decreased SNB (B=-0.94, p = 0.036), increased ANB (B = 0.74, p = 0.014) and increased MP/SN (B = 2.22, p < 0.001). Similarly, children with adenotonsillar hypertrophy correlated with decreased SNB (B=-1.36, p = 0.015), increased ANB (B = 1.35, p < 0.001) and increased MP/SN (B = 2.64, p = 0.001).
CONCLUSIONS
Isolated adenoid hypertrophy correlated with a retrognathic mandible, an increased maxillo-mandibular sagittal discrepancy, and an increased mandibular plane angle. Isolated tonsillar hypertrophy correlated with maxillary and mandibular protrusion. Adenotonsillar hypertrophy did not show a superimposed craniofacial pattern of the above two but showed the same craniofacial pattern as isolated adenoid hypertrophy.
Topics: Male; Child; Female; Humans; Palatine Tonsil; Adenoids; Mandible; Hypertrophy; Cephalometry
PubMed: 37024864
DOI: 10.1186/s12887-023-03979-2