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At least 19 recordsLinked to original sources

PubMed1978

[The heart in hypertension. V. Systolic and diastolic wall stress and degree of hypertrophy as determinants of diagnostic and therapeutical consequences (author's transl)].

The appropriateness of hypertrophy was analyzed in 64 patients with essential hypertension during diagnostic cardiac catheterization and left ventriculography. The degree of hypertrophy may be described by the relationships between peak systolic pressure, mass to volume ratio and peak systolic wall stress. The peak systolic wall stress represents an important determinant of the appropriateness of hypertrophy and has great influence on left ventricular function and myocardial energy demand. The hypertrophy in essential hypertension may be subdivided into 3 different types of hypertrophy: (a) inappropriate hypertrophy associated with increased mass-to-volume ratio and decreased systolic wall stress, (b) appropriate hypertrophy with normal systolic wall stress and (c) inappropriate hypertrophy with normal or decreased mass-to-volume ratio, however with significantly increased systolic wall stress. On the basis of the appropriateness or degree of left ventricular hypertrophy in essential hypertension the therapeutical consequences are being discussed with special reference to beta receptor blockade and digitalis glycosides.

Adrenergic beta-Antagonists↗

PubMed1979

Cardiac hypertrophy in early hypertension.

Studies of cardiac hypertrophy in spontaneously hypertensive rats have indicated that left ventricular hypertrophy occurred even in the prehypertensive stage. These findings suggested that other factors besides blood pressure levels, and including possibly a genetic predisposition to myocardial hypertrophy, could play a role in structural cardiovascular alterations in spontaneously hypertensive rats. More recent studies have confirmed these anatomic results; left ventricular hypertrophy was vectorcardiographically detected even in the prehypertensive stage in voth young stroke-prone rats and stroke-resistant spontaneously hypertensive rats. Further, a close relation was found between degree of left ventricular hypertrophy and vascular hypertrophy or hyperplasia; this suggests that early detection of left ventricular hypertrophy may be a useful indicator of the incipient stage of structural vascular changes in genetic hypertension.

Adrenergic beta-Agonists↗

PubMed2025

Cardiac hypertrophy at the crossroads: Mechanistic insights and emerging multimodal therapeutic strategies.

Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide, accounting for approximately 17.9 million deaths annually. Among their diverse manifestations, cardiac hypertrophy is a clinically significant condition that predisposes patients to heart failure, arrhythmias, and and sudden cardiac death. Clinically, hypertrophy can be classified into three forms: physiological (adaptive) hypertrophy, which supports cardiac performance and is reversible, pathological hypertrophy most often secondary to hypertension, valvular disease, hemodynamic stress, or sustained neurohumoral activation; and hypertrophic cardiomyopathy (HCM) represents a primary genetic disorder, most often caused by mutations in sarcomeric proteins. These distinct etiologies have important therapeutic implications, as they determine how efficiently pharmacological agents can target underlying mechanisms. Conventional pharmacological treatments are widely used in clinical practice, yet they provide limited reversal of established remodeling. This therapeutic gap has driven the development of innovative modalities such as RNA-based therapeutics, exosome-mediated interventions, stem cell-derived therapies, and genome-editing technologies, which aim to modulate maladaptive signaling and restore myocardial integrity. This review integrates clinical perspectives with mechanistic insights, delineating the drivers of pathological hypertrophy while evaluating both established therapies and emerging strategies that hold promise for precision cardiology and improved patient outcomes.

Humans↗

PubMed1979

Regression of left ventricular hypertrophy during treatment with antihypertensive agents.

1 Echocardiography showed 14 of 24 patients with essential hypertension to have hypertrophy of their left ventricular walls. In eight of these 14 patients the left ventricular configuration initially fulfilled the criteria for asymmetric septal hypertrophy (ASH) and six were symmetrically hypertrophied, the remaining ten being normal. 2 Following 12 weeks' treatment of hypertension with the object of reducing the supine BP to 150/90 mmHg or below, there was a reduction of wall thickness so that only two of the eight continued to show ASH. 3 The six patients with symmetrical left ventricular hypertrophy also showed a significant reduction in the thickness of the septum and the posterior wall. Those with normal echocardiograms did not change. 4 This reduction of wall thickness produced by antihypertensive therapy may represent regression of left ventricular hypertrophy.

Adrenergic beta-Antagonists↗

PubMed2026

Phosphoproteomics identification of ERK-dependent activation of Rps6kb1 in cardiac hypertrophy.

Cardiomyocyte growth is tightly controlled by multiple signaling pathways. Identification of master kinases in this process is essential in exploring potential targets for the treatment of pathological cardiac hypertrophy and heart failure. Here we identified the mTOR-independent activation of ribosomal protein S6 kinase b1 (Rps6kb1) during cardiomyocyte growth. By utilizing phosphoproteomics in primary neonatal rat ventricular myocytes, we revealed Rps6kb1 as one of most activated kinases under growth stimulation. We further demonstrated the role of Rps6kb1 phosphorylation in pathological cardiac hypertrophy and heart failure. We showed that the phosphorylation of multiple sites in Rps6kb1, including T367 in the kinase domain and S418/T421/S424 in the C-terminal domain, is not directly regulated by the activity of mTOR but coupled with the activation of the MEK1/ERK axis. In mice, cardiomyocyte-specific deletion of Rps6kb1 significantly inhibited both constitutively active ERK- and pressure overload-induced cardiac hypertrophy. In contrast, cardiomyocyte-specific overexpression of wild-type Rps6kb1, rather than the phosphorylation-defective mutant, elevated cardiac hypertrophy and augmented pressure overload-induced heart failure. In conclusion, our findings reveal that the MEK/ERK axis primes Rps6kb1 activation through phosphorylation of 2 separate domains of Rps6kb1, which may play an essential role in cardiac hypertrophy and heart failure under hemodynamic stress.

Animals↗

PubMed1976

Cyclic nucleotide metabolism in compensatory renal hypertrophy and neonatal kidney growth.

Cyclic nucleotide metabolism was investigated in growing kidneys of rats during compensatory hypertrophy and during neonatal development. After unilateral nephrectomy a mild and short-lasting decrease in cyclic 3':5" adenosine monophosphate (cAMP) was observed in the hypertrophying kidney. In contrast, cyclic 3':5' guanosine monophosphate (cGMP) showed a sharp decline to 20% of control at 15 min and a rapid rise to 200-300% above base-line at 1-72 hr. The alterations in renal tissue levels of cGMP were associated with parallel changes in the soluble, 100,000 X g supernatant guanylate cyclase activity [GTP pyrophosphate-lyase (cyclizing): EC 4.6.1.2]. No change was observed in total cGMP phosphodiesterase (3':5'-cyclic-nucleotide 5'-nucleotidohydrolase; EC 3.1.4.17). In the rapidly growing kidney of newborn rats cAMP levels were 983 +/- 65 and 833 +/- 42 pmol/g of kidney at 4 and 7 days after birth, and increased to adult levels (1518 +/- 57 pmol/g) at 21 days whereas cGMP levels were 59.8 +/- 6.8 and 92.5 +/- 13.9 pmol/g at 4 and 7 days and decreased to adult levels (36 +/- 1.5) at 21 days. The results indicate that compensatory renal hypertrophy and neonatal kidney growth are associated with changes in cAMP and cGMP metabolism.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1977

Development of SHR hypertension and cardiac hypertrophy during prolonged beta blockade.

Spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were treated with beta-adrenergic receptor inhibiting drugs (either propranolol or timolol) from conception until 12 weeks of age to determine if this therapy would alter the development of systemic hypertension or left ventricular hypertrophy. Therapy (propranolol or timolol, 500 mg/liter drinking water) was initiated with breeding parents and continued throughout the pregnancy, nursing, and postweaning periods. Although the heart rates of beta-adrenergic receptor inhibited WKY and SHR rats were consistently reduced with respect to their respective tap-water controls, this therapy did not alter body growth. Hemodynamic studies demonstrated reduced central venous pressure, cardiac index, and maximum acceleration of aortic flow in the beta-adrenergic inhibited rats. In spite of these findings, the arterial pressure of the treated rats and the degree of left ventricular hypertrophy of the SHR were unaltered by treatment. Thus, administration of the beta-adrenergic receptor blocking agents, propranolol or timolol, from conception through the developmental stage of SHR hypertension, failed to alter either the progressive rise in arterial pressure or the development of hypertensive vascular disease and left ventricular hypertrophy.

Adrenergic beta-Antagonists↗

PubMed2026

Left ventricular hypertrophy in hypertension: a systematic review and meta-analysis of echocardiographic studies published from 2011 to 2025.

AIM: An updated meta-analysis targeting the prevalence of left ventricular hypertrophy (LVH), a cardinal marker of hypertensive heart disease (HHD), over the last 15 years is lacking. Thus, we analyzed the literature in order to provide a comprehensive information on LVH prevalence, as assessed by echocardiography, in the hypertensive setting. METHODS: The PubMed, OVID-MEDLINE, and Cochrane Library databases were analyzed to search English-language articles published from 1 January 2011 up to 31 December 2025. Studies were identified by using MeSH terms and crossing the following search items: 'left ventricular hypertrophy', 'left ventricular mass', 'hypertensive heart disease', 'echocardiography', 'hypertension', and 'subclinical cardiac damage'. RESULTS: A total of 51 studies including 74 632 hypertensive patients were considered. Overall, the prevalence of LVH in the pooled cohort, defined according to criteria recommended by echocardiographic guidelines, was 36.6% (95% CI: 33.4-40%). Data provided by 18 studies ( n  = 40 108 patients) showed that the probability of having LVH was lower in men than in women (OR = 0.62, CI: 0.48-0.80, P  < 0.0001). Among patients with LVH (17 studies), the risk of concentric LVH was almost twice as high as eccentric (OR = 1.94, CI: 1.52-2.49, P  < 0.0001). CONCLUSION: Our meta-analysis suggests that the high contemporary prevalence of LVH reflects the failure of therapeutic strategies worldwide in the prevention and treatment of HHD. From a clinical perspective, these data imply the need for a more aggressive treatment of hypertension and related cardiovascular risk factors leading to LVH, especially in women.

Humans↗

PubMed1979

[Echocardiographic diagnosis of obstructive myocardiopathies: study of the systolic anterior motion of the mitral valve and septal hypertrophy as compared with the hemodynamic and mechanographic findings. Evolution under medical treatment].

Characteristic echocardiographic features of hypertrophic obstructive cardiomyopathy were recorded in 24 patients, all of whom had asymmetric septal hypertrophy and systolic anterior motion of the mitral valve (SAM) at rest or after pharmacodynamic stimulation. The relationship between outflow tract obstruction and SAM was assessed by comparison with data obtained at cardiac catheterisation and external mechanography: SAM seems to be a non-specific phenomenon and may be recorded in cases of hypertrophic cardiomyopathy without obstruction during pharmacodynamic stimulation. In forms with obstruction, SAM and the severity of obstruction increase with the degree of spetal hypertrophy. The increased contractility of the left ventricular posterior wall appears to be an important factor in the mechanism of SAM which can be prevented by betablockade in moderate or labile forms. When SAM is permanent, whatever the gradient recorded, it is a sign of anatomical deformation of the left ventricle and may be an additional indication for cardiac surgery.

Adrenergic beta-Antagonists↗

PubMed1976

Enhancement of sulphatide metabolism in the hypertrophied kidney of C3H/He mouse with reference to [Na+, K+]-dependent ATPase.

Sulphatide (cerebroside sulphate) metabolism of C3H/He mouse kidney was investigated in the course of compensatory renal hypertrophy in association with the change of [Na+,K+]-dependent ATPase, arylsulfatase A and beta-galactosidase activity. A remarkable increase in 35S incorporation into kidney sulphatide was observed 24 hours and especially 7 days after unilateral nephrectomy. In contrast, no significant alteration of 32P incorporation into major phospholipids such as phosphatidylcholine, phosphatidylethanolamine and sphingomyelin was demonstrated in the compensatory hypertrophied mouse kidney. [Na+, K+]-dependent ATPase increased to 126% of control in the remaining kidneys on 7 days after operation. Specific increase in 35S specific activity of kidney sulphatide suggests its possible link with the process of active ion transport through membrane-bound [Na+,K+]-dependent ATPase. Arylsulphatase A activity increased to 151% of control on days, while little change was observed in beta-galactosidase activity. These results suggest a sole concern of a turnover of sulphate moiety of sulphatide molecule in the elevated metabolism.

Adenosine Triphosphatases↗

PubMedDate not supplied

The effect of beta adrenergic blockade on pulmonary hypertension, right ventricular hypertrophy and polycythaemia, induced in rats by intermittent high altitude hypoxia.

Adult male rats were used to study the effect of a beta blocking agent on pulmonary hypertension and right ventricular hypertrophy induced by intermittent high altitude (IHA) hypoxia (8 hr daily, 5 days a week, stepwise up to the simulated altitude of 7000 m). Trimepranol was injected subcutaneously in a single dose of 10 mg/kg/b.w. one hour before each IHA exposure. Administration of the beta blocking drug caused significant changes of haematocrit values even in animals kept under normoxic conditions. The initial deep decrease was followed by a slow return to control values; prolongation of treatment led to a further significant decrease of the haematocrit curve. The polycythaemic response of IHA-exposed and Trimepranol-treated animals was, therefore, significantly less pronounced as compared with the hypoxic non-treated group. Administration of Trimepranol to IHA-exposed rats significantly decreased the values of right ventricular systolic and mean pressure, right ventricular hypertrophy as well as the degree of muscularization of pulmonary arteries. It may be assumed that the protective effect of Trimepranol is due to a) changes in pulmonary vascularization, b) reduction of polycythaemia, and c) lower cardiac output, induced by the negative inotropic and chronotropic effect of this drug.

Altitude Sickness↗

PubMed2026

Proteomics combined with single-cell sequencing reveals key genes and computational lead compound related to ligamentum flavum hypertrophy, lactate metabolism and lactate modification.

Ligamentum flavum hypertrophy (LFH) is a hallmark pathological feature of lumbar spinal stenosis; however, its underlying molecular mechanisms remain incompletely understood. Lactate metabolism and related lactylation modifications have emerged as critical links between cellular metabolism and epigenetic regulation, with established roles in various fibrotic and inflammatory diseases. Nevertheless, the specific contribution of lactylation to LFH pathogenesis remains unexplored. In this study, we integrated proteomic profiling of ligamentum flavum tissues with single-cell transcriptomic data to identify differentially expressed proteins associated with LFH. Cross-referencing these genes with genes involved in lactate metabolism and lactylation yielded 16 candidate genes. Through functional enrichment analysis, protein-protein interaction network construction, and GraphBAN model prediction, we identified five hub genes (NDUFS2, HMOX1, SPR, FABP5, and PFKP) and two potential lead compounds (ZINC000014879975 and ZINC000242437513). Molecular docking analysis confirmed favorable binding affinities between these compounds, suggesting that they may serve as potential lead compounds worthy of further experimental investigation. Single-cell analysis further revealed that macrophages occupy a central position in the LFH microenvironment, resulting in pronounced metabolic reprogramming and remodeling of intercellular communication networks, particularly via the MIF-CD74/CD44 axis, under pathological conditions.

Proteomics↗

PubMed1978

Unilateral cryptorchidism with compensatory hypertrophy of descended testicle in prepubertal boys.

5 prepubertal boys with unilateral cryptorchidism and compensatory hypertrophy of the descended testicle, 22 prepubertal boys with unilateral cryptorchidism and without CTH, and 14 prepubertal normal boys were submitted to LH-RH and to HCG tests in order to study the hormonal behaviour in CTH phenomenon before puberty. High but normal peaks of plasma LH and FSH were observed after LH-RH in CTH boys who showed a significant increase of testosterone after HCG stimulation. On the contrary the LH response to LH-RH and the testosterone response to HCG of the boys with unilateral cryptorchidism and without CTH were, as expected, significantly lower than in the control ones.

Child, Preschool↗

PubMed1977

Different effects of amygdaloid lesions on compensatory ovarian hypertrophy in cyclic and prepubertal female rats.

Cyclic and 28-day-old immature female rats were hemiovariectomized and partly bilaterally lesioned in the cortical amygdaloid nucleus (CAN). The compensatory ovarian hypertrophy (COH) recorded in the adult females on the 8th day after hemicastration was completely prevented by the amygdaloid lesions. In contrast, damage to the CAN did not alter the ovarian weight in prepubertal females, although COH was also induced in these animals by unilateral ovariectomy.

Amygdala↗

PubMed1978

Pharmacological study of cholinergic mechanisms of compensatory ovarian hypertrophy in rats.

Treatment of hemicastrated adult female rats with nicotine increased the compensatory ovarian hypertrophy (COH) while central n-cholinolytic IEM-506 decreased COH and prevented the estrogen-induced suppression of COH. Administration of L-DOPA abolished the effect of IEM-506, and disulfiram blocked gonadotropic action of nicotine. Elevation of the dose of arecoline decreased COH and the sensitivity of hypothalamo-gonadotropic complex to estrogen suppression. Treatment of rats with L-DOPA and disulfiram abolished the late effect of arecoline. Central m-cholinolytic metamizyl decreased COH, potentiated the effect of estrogen and prevented the gonadotropic effect of L-DOPA. The regulatory role of m-cholinergic systems in noradrenaline mediation of gonadotropic function and n-cholinergic system in dopamine ones are suggested.

Animals↗

PubMed2026

Colchicine attenuates cardiac hypertrophy by targeting the macrophage-driven Interleukin-6 suppression.

Hypertrophic cardiomyopathy (HCM), the most prevalent inherited cardiovascular disease, is strongly linked to progressive heart failure and sudden cardiac death (SCD). However, its underlying pathogenic mechanisms remain incompletely understood, and effective therapeutic strategies are still lacking. Here, we established two murine HCM models harboring high SCD risk-associated mutations. Single-cell RNA sequencing revealed immune activation and enhanced fibrotic remodeling in the myocardium of these models. Therefore, we hypothesized that colchicine, a widely used anti-inflammatory drug known to reduce cardiovascular events in multiple cardiac disorders, may also represent a promising therapeutic candidate for HCM. As we expected, colchicine treatment attenuated pathological remodeling in our study, as evidenced by reduced cardiomyocyte hypertrophy, decreased fibrosis, and downregulation of cardiac stress markers (Anp, Bnp) and fibrotic mediators (Ctgf, Col1a1, Col3a1). In addition, colchicine attenuated pro-inflammatory macrophage populations and suppressed IL-6 expression, thereby contributing to the preservation of cardiac function. These findings provide the first preclinical evidence that colchicine alleviates myocardial inflammation and fibrosis in HCM, underscoring its potential as a novel therapeutic strategy to reduce fibrosis, lower SCD risk, and improve patient outcomes.

Animals↗

PubMed2025

A deep insight into the sialome of the house fly, Musca domestica, infected with the salivary gland hypertrophy virus (MdSGHV).

The house fly, Musca domestica, serves as a mechanical vector for numerous pathogens, posing a significant risk to human and animal health. More than two decades ago, the Musca domestica salivary gland hypertrophy virus (MdSGHV) was discovered, infecting both males and females flies and disrupting mating and the reproductive process. While MdSGHV can infect various tissues, its primary replication site is the house fly salivary gland. It is well established that arthropod salivary glands play an important role not only in acquiring food but also in transmitting pathogens. Therefore, understanding the composition of vector salivary glands and the interactions between vector and pathogen components is essential for developing future control strategies. To this end, we conducted a comprehensive RNA-sequencing of salivary glands from both infected and non-infected house flies. Our analysis identified a total of 6,410 putative sequences, with 6,309 originating from M. domestica and 101 from the MdSGHV, categorized into 25 functional groups. Furthermore, differential expression analysis between infected and non-infected salivary glands revealed 2,852 significantly modulated transcripts, highlighting profound transcriptional changes triggered by MdSGHV infection. Overall, these findings not only deepen our understanding of the composition of M. domestica salivary glands but also provide valuable insight into the virus-vector interaction, which could serve as a model to understand other medically relevant interactions.

Salivary Glands↗

PubMed2025

Scalable Deep Learning of Histology Images Reveals Genetic and Phenotypic Determinants of Adipocyte Hypertrophy.

BACKGROUND: White adipose tissue dysfunction has emerged as a critical factor in cardiometabolic disease development, yet the cellular microstructure and genetic architecture of adipocyte morphology remain poorly explored. METHODS: We introduce Adipocyte U-Net 2.0, an advanced deep learning method for the semantic segmentation of adipose tissue histology, enabling analysis of over 27 million adipocytes from 2,667 individuals. FINDINGS: Our approach revealed that adipocyte hypertrophy associates with metabolic dysfunction, including increased fasting glucose, glycated hemoglobin, leptin, and triglycerides, with decreased adiponectin and HDL cholesterol levels. Through the largest genome-wide association study of adipocyte size to date (NSubcutaneous = 2,066, NVisceral = 1,878), we identified four genome-wide significant loci: two in sex-combined analysis (rs73184721 in NAALADL2 and rs200047724 in NRXN3) and two female-specific variants (rs140503338 and rs11656704 in ULK2). Notably, these genetic associations showed congruent relationships with cardiometabolic traits, suggesting shared biological mechanisms. INTERPRETATION: Our findings demonstrate the utility of deep learning for adipocyte phenotyping at scale and provide novel insights into the genetic basis of adipocyte morphology and its relationship to metabolic disease.

Journal Article↗