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Heribert Schunkert

Publications and source records attributed to Heribert Schunkert.

At least 19 recordsLinked to original sources
PubMed2026

Genetic screening of children for familial hypercholesterolaemia: the VRONI study.

BACKGROUND AND AIMS: The role of genetic testing as part of universal screening programmes for familial hypercholesterolaemia (FH) in children is not well defined. Here, a two-step approach to identify children carrying FH-causing variants was investigated. METHODS: In this study from Southern Germany, paediatricians were invited to offer FH screening to all children aged 4.8-14.9 years at routine paediatric examinations. The FH screening programme began in September 2020 in Bavaria and has involved up to 480 paediatricians. It included biochemical and genetic testing using 0.2 mL of blood taken from a fingertip. In case of low-density lipoprotein cholesterol (LDL-C) serum concentration ≥3.36 mmol/L (≥130 mg/dL), FH-causing variants were determined in the same sample with a focused panel covering most frequent variants (n = 48) and sequencing of relevant genes. RESULTS: Out of 25 431 children screened so far, 1689 children had an LDL-C ≥ 3.36 mmol/L (>130 mg/dL), which defined this concentration as the 93rd percentile. Pathogenic variants were identified by the focused panel in 157 and by next-generation sequencing in 283 children, respectively. While 17% (283/1670) of all genetically analysed children tested positive, the fraction of individuals with FH-causing variants increased across the spectrum of LDL-C serum concentrations from 4.7% (23/492) at 3.36-3.49 mmol/L (130-135 mg/dL) to 78.6% (81/103) above 5.17 mmol/L (200 mg/dL). Overall, the prevalence of FH-causing variants was high (1:90). One reason was a founder variant (n = 63) within the LDLR gene, found 40 times more frequent than European average. The analysis of recruitment data revealed significant ascertainment bias, with lower recruitment rate practices exhibiting higher prevalence. After adjustment for the bias using a generalized linear mixed model, the predicted prevalence was 1 in 163 (0.61%), which is highly consistent with large-scale genomic benchmarks as gnomAD (1:165, n = 622 057) and the UK Biobank (1:176, n = 48 741). CONCLUSIONS: The prevalence of FH determined in this study is significantly higher than previously published estimates (∼1:250), highlighting the importance of this condition for public health and supporting calls for a national paediatric screening programme, given the availability of effective treatment options. For children between 5 and 15 years, biochemical screening is an effective way to select patients for genetic testing, with sequencing of candidate genes being superior to variant screening. In summary, the VRONI study demonstrates the feasibility and efficacy of a combined biochemical and genetic screening for FH in children.

Humans↗
PubMed2025

Distinct Genetic Risk Profile in Aortic Stenosis Compared With Coronary Artery Disease.

IMPORTANCE: Aortic stenosis (AS) and coronary artery disease (CAD) frequently coexist. However, it is unknown which genetic and cardiovascular risk factors might be AS-specific and which could be shared between AS and CAD. OBJECTIVE: To identify genetic risk loci and cardiovascular risk factors with AS-specific associations. DESIGN, SETTING, AND PARTICIPANTS: This was a genomewide association study (GWAS) of AS adjusted for CAD with participants from the European Consortium for the Genetics of Aortic Stenosis (EGAS) (recruited 2000-2020), UK Biobank (recruited 2006-2010), Estonian Biobank (recruited 1997-2019), and FinnGen (recruited 1964-2019). EGAS participants were collected from 7 sites across Europe. All participants were of European ancestry, and information on comorbid CAD was available for all participants. Follow-up analyses with GWAS data on cardiovascular traits and tissue transcriptome data were also performed. Data were analyzed from October 2022 to July 2023. EXPOSURES: Genetic variants. MAIN OUTCOMES AND MEASURES: Cardiovascular traits associated with AS adjusted for CAD. Replication was performed in 2 independent AS GWAS cohorts. RESULTS: A total of 18 792 participants with AS and 434 249 control participants were included in this GWAS adjusted for CAD. The analysis found 17 AS risk loci, including 5 loci with novel and independently replicated associations (RNF114A, AFAP1, PDGFRA, ADAMTS7, HAO1). Of all 17 associated loci, 11 were associated with risk specifically for AS and were not associated with CAD (ALPL, PALMD, PRRX1, RNF144A, MECOM, AFAP1, PDGFRA, IL6, TPCN2, NLRP6, HAO1). Concordantly, this study revealed only a moderate genetic correlation of 0.15 (SE, 0.05) between AS and CAD (P = 1.60 × 10-3). Mendelian randomization revealed that serum phosphate was an AS-specific risk factor that was absent in CAD (AS: odds ratio [OR], 1.20; 95% CI, 1.11-1.31; P = 1.27 × 10-5; CAD: OR, 0.97; 95% CI 0.94-1.00; P = .04). Mendelian randomization also found that blood pressure, body mass index, and cholesterol metabolism had substantially lesser associations with AS compared with CAD. Pathway and transcriptome enrichment analyses revealed biological processes and tissues relevant for AS development. CONCLUSIONS AND RELEVANCE: This GWAS adjusted for CAD found a distinct genetic risk profile for AS at the single-marker and polygenic level. These findings provide new targets for future AS research.

Humans↗
PubMed2006

Mild therapeutic hypothermia after cardiac arrest - a nationwide survey on the implementation of the ILCOR guidelines in German intensive care units.

AIM: To investigate the implementation of mild therapeutic hypothermia (MTH) after cardiac arrest into clinical practice. METHODS AND RESULTS: A structured evaluation questionnaire was sent to all German hospitals registered to have ICUs; 58% completed the survey. A total of 93 ICUs (24%) reported to use MTH. Of those, 93% started MTH in patients after out-of-hospital resuscitation with observed ventricular fibrillation and 72% when other initial rhythms were observed. Only a minority of ICUs initiate MTH in patients after cardiac arrest with cardiogenic shock (28%), whereas 48% regarded cardiogenic shock as a contra-indication for MTH. On average, target temperature was 33.1+/-0.6 degrees C and duration of cooling 22.9+/-4.9 h. Many centres used economically priced cold packs (82%) and cold infusions (80%) for cooling. The majority of the ICUs considered infection, hypotension and bleeding as relevant complications of hypothermia which was of therapeutic relevance in less than 25% of the cases. CONCLUSIONS: MTH is underused in German ICUs. Centres which use MTH widely follow the recommendations of ILCOR with respect to the indication and timing of cooling. In hospitals that use MTH the technique is considered to be safe and inexpensive. More efforts are needed to promote this therapeutic option and hypothermia since MTH has now been included into European advanced cardiovascular life support protocols.

Cardiopulmonary Resuscitation↗
PubMed2006

Modulation of ventricular repolarization in patients with transient left ventricular apical ballooning: a case control study.

OBJECTIVE: Even though diffuse T wave inversion and prolongation of the QT interval in the surface electrocardiogram (ECG) have been consistently reported in patients with transient stress-induced left ventricular apical ballooning (AB), ventricular repolarization has not yet been systematically investigated in this clinical entity. BACKGROUND: AB, an emerging syndrome that mimics acute ST-segment elevation myocardial infarction (MI), is characterized by reversible left ventricular wall motion abnormalities in the absence of obstructive coronary heart disease and significant QT interval prolongation. METHODS: We prospectively enrolled 22 consecutive patients (21 women, median age 65 years) with transient left ventricular AB. A total of 22 age-, gender-, body-mass-index-, and left-ventricular-function-matched patients with acute anterior ST-segment elevation MI undergoing successful direct percutaneous coronary intervention for a proximal occlusion of the LAD, as well as 22 healthy volunteers served as control groups. Beat-to-beat QT interval and QT interval dynamicity were determined from 24-hour Holter ECGs, recorded on the third day after hospital admission. RESULTS: There were no significant differences in baseline clinical characteristics, except higher peak enzyme release in MI patients. Compared with MI patients, AB patients exhibited significantly prolonged mean QT intervals and rate-corrected QT intervals (QT: 418 +/- 37 vs 384 +/- 33 msec, P < 0.01; QTcBazett: 446 +/- 40 vs 424 +/- 35 msec, P < 0.05; QTcFridericia: 437 +/- 35 vs 412 +/- 31 msec, P < 0.05). Mean RR intervals tended to be higher in AB patients, without reaching statistical significance (877 +/- 96 vs 831 +/- 102 msec, P = NS). The linear regression slope of QT intervals plotted against RR intervals was significantly flatter in AB patients at both day- and nighttime (QT/RR slopeday: 0.18 +/- 0.04 vs 0.22 +/- 0.06, P < 0.01; QT/RR slopenight: 0.12 +/- 0.03 vs 0.17 +/- 0.05, P < 0.01). CONCLUSION: The present study is the first to demonstrate significant differences of QT interval modulation in patients with transient left ventricular AB and acute ST-segment elevation MI. Even though transient AB is associated with a significant QT interval prolongation, rate adaptation of ventricular repolarization (i.e., QT dynamicity) is not significantly altered, suggesting a differential effect of autonomic nervous activity on the ventricular myocardium in transient AB and in acute MI.

Aged↗
PubMed2006

Genetics and heritability of coronary artery disease and myocardial infarction.

A positive family history is frequently reported by patients with coronary artery disease (CAD) or myocardial infarction. For risk stratification, it is crucial to distinguish between accidental reoccurrence of sporadic cases and cases with a true heritable component of the conditions. A familial predisposition is assumed when a myocardial infarction is diagnosed by a male first degree relative before the 55th year of life or a female first degree relative before the 65th year of life. The current manuscript reviews major studies from which a familial risk of CAD or myocardial infarction can be inferred. Moreover, a brief overview summarizes the current results of molecular genetic research on chromosomal loci and genes relevant for CAD and myocardial infarction.

Coronary Artery Disease↗
PubMed2006

Comparison of coronary restenosis rates in matched patients with versus without diabetes mellitus.

Diabetes mellitus (DM) is an established risk factor for stent restenosis, in part as a result of the smaller vessel dimensions and longer lesions. This study compared the magnitude of acute lumen gain and late lumen loss after elective coronary stent implantation in patients with and without DM using a matched-pair analysis. A total of 133 patients with DM and 192 coronary lesions were included in this analysis. A group of 192 lesions in 182 patients without DM were matched in a pairwise fashion, stratifying for reference diameter, minimal luminal diameter, and lesion length. The binary restenosis rate at the 5-month follow-up angiography was 25% in the DM group and 14% in the non-DM group (p <0.01). Acute angiographic lumen gain (1.47 +/- 0.41 vs 1.56 +/- 0.38 mm, p = 0.03) and late lumen loss (0.64 +/- 0.42 vs 0.55 +/- 0.36 mm, p = 0.02) were significantly different between the DM and non-DM groups. In conclusion, suboptimal acute procedural results and an exaggerated neointimal proliferation contributed by about 50% to the lower net lumen gain in the DM group. Patients with DM had a significantly higher restenosis rate even when matched for preprocedural angiographic lesion dimensions. Mechanistically, inferior procedural results, as well as exaggerated neointimal proliferation, are, quantitatively, equally important in this process.

Aged↗
PubMed2006

Ultrafine mapping of Dyscalc1 to an 80-kb chromosomal segment on chromosome 7 in mice susceptible for dystrophic calcification.

In mice, dystrophic cardiovascular calcification (DCC) is controlled by a major locus on proximal mouse chromosome 7 named Dyscalc1. Here we present a strategy that combines in silico analysis, expression analysis, and extensive sequencing for ultrafine mapping of the Dyscalc1 locus. We subjected 15 laboratory mouse strains to freeze-thaw injury of the heart, and association with respective genotypes allowed condensation of the Dyscalc1 locus to 1 Mb. Within this region, 51 known and predicted genes were studied in DCC-susceptible C3H/He and DCC-resistant C57BL/6 mice with respect to mRNA expression in response to injury. Five genes displayed differential expression. Genotyping of seven novel single nucleotide polymorphisms (SNPs) within these genes revealed an 80-Kb region in NZB mice that were found positive for calcification though carrying otherwise alleles from DCC-resistant mice. This microheterogeneity in NZB mice was evolutionary conserved in all DCC-susceptible mouse strains and contains the genes EMP-3, BC013491, and Abcc6 (partially). The flanking SNPs are rs3703247 and NT_039420.5_2757991. mRNA levels of EMP-3 were found to be upregulated in response to injury in both C57BL/6 and C3H/He mice. Sequencing of EMP-3 revealed an SNP leading to an amino acid substitution (p.T153I) that was found in all mouse strains susceptible for DCC but not in resistant strains such as C57BL/6 mice. Thus, the p.T153I changes might affect the biological function of EMP-3 gene product after injury. Using this combined approach, we ultrafine-mapped the Dyscalc1 locus to an 80-Kb region and identified EMP-3 as a new candidate gene for DCC.

Animals↗
PubMed2006

Association of low-grade urinary albumin excretion with left ventricular hypertrophy in the general population: the MONICA/KORA Augsburg Echocardiographic Substudy.

BACKGROUND: Even mild renal dysfunction is a predictor of cardiovascular morbidity. We investigated whether sub-threshold microalbuminuria or mildly decreased estimated glomerular filtration rate (eGFR) are related to left ventricular hypertrophy (LVH) in the general population. METHODS: Urinary albumin-to-creatinine ratio (UACR) served to determine albuminuria, eGFR was estimated using modification of diet in renal disease (MDRD) formula, and LV geometry was assessed echocardiographically in the third MONItoring of trends and determinants in CArdiovascular disease/Cooperative Health Research in the Augsburg Area (MONICA/KORA) Augsburg survey (n = 1187). RESULTS: The prevalence of LVH increased in parallel with UACR. Compared with the first tertile of this normal population, the age, systolic blood pressure (SBP), body mass index, gender and diabetes adjusted odds ratio (OR) for LVH was elevated already in the second (4.32-8.75 mg/g in men; 4.60-9.48 mg/g in women; OR: 2.10, P = 0.001) as well as in the third UACR-tertile (> or =8.76 mg/g in men; > or =9.49 mg/g in women; OR: 1.63, P = 0.035). Likewise, adjusted SBP increased with UACR-tertiles [129 vs 132 (P = 0.036) and 137 mmHg (P < 0.001) in the first, second and third tertile, respectively], whereas diastolic blood pressure was significantly elevated only in the third UACR-tertile [79 vs 80 and 81 mmHg (P = 0.002) in the tertiles, respectively]. In contrast, tertiles of eGFR or mildly impaired eGFR (<90 ml/min/1.73 m(2)) were not associated with the prevalence of LVH in multivariate models. CONCLUSIONS: At the general population level, even low-grade albuminuria is associated with LVH. Thus, the conventional UACR-threshold of microalbuminuria (30 mg/g) may be too conservative given that end organ damage such as LVH is observed with increased frequency at much lower levels.

Adult↗
PubMed2006

Novel missense mutations (p.T596M and p.P1797H) in NOTCH1 in patients with bicuspid aortic valve.

The bicuspid aortic valve (BAV) is the most common congenital cardiac malformation, occurring in 1-2% of the population. In a recent report, mutations in NOTCH1 a signaling and transcriptional regulator have been shown to cause BAV in two families. This study provides data on systematic sequencing in search for novel mutations in NOTCH1 gene in a large sample BAV. For the first time, we report results of a systematic mutation-analysis based on DNA-sequencing of all coding exons and adjacent splice consensus sequences of NOTCH1 gene. Our analyses revealed 57 NOTCH1 sequence variants. Twenty-one variants are located within exons and 36 within intronic or 5'-UTR sequences. Thirty-five variants were described previously as polymorphisms. The remaining 22, however, were neither listed in public SNP databases nor in the literature and were therefore considered novel. Seventeen variants were found only once (MAF = 1%), of these 15 were novel. Two sequence variants led to amino acid substitutions (p.T596M and p.P1797H) and are located in highly conserved regions of the NOTCH1 protein. In addition, these two mutations could not be detected in at least 327 healthy controls by using RFLP-analysis. The functional relevance of the other 13 novel and rare variants could not be proven without further functional examination. In this study, we provide a new evidence that the mutations in the NOTCH1 gene may trigger the underlying mechanism causing the valve calcification, especially in BAV. In conclusion, NOTCH1 gene mutations do not only play a role in familiar BAV, but can also be observed in approximately 4% of sporadic cases.

Adult↗
PubMed2006

Association of the Ghrelin receptor gene region with left ventricular hypertrophy in the general population: results of the MONICA/KORA Augsburg Echocardiographic Substudy.

Growth hormone (GH) can influence left ventricular myocardial growth, structure, and function. The GH secretagogue receptor (GHSR, ghrelin receptor) is known to be involved in GH release and is expressed in the myocardium. We hypothesized that genetic variants within the GHSR are associated with parameters of left ventricular mass (LVM) and geometry. Ten single-nucleotide polymorphisms (SNPs) covering the gene region were genotyped in 1230 members of the general population (Monitoring Trends and Determinants on Cardiovascular Diseases Augsburg Echocardiographic Substudy). Linkage disequilibrium analysis revealed a linkage disequilibrium block consisting of 5 SNPs forming 2 common haplotypes. One haplotype was found significantly more often in subjects without left ventricular hypertrophy ([LVH] 69% versus 59%; permutated P=0.0015), whereas the second haplotype was significantly more frequent in individuals with LVH (32% versus 26%; P=0.019). Homozygous subjects presented with an increase of risk with respect to all heart size parameters. A significantly increasing frequency of the risk haplotype could be observed from the lowest (20.9%) to the highest quintile (31.0%) of gender-specific LVM distributions (P=0.0096). We found association of the minor alleles of individual single nucleotide polymorphisms contributing to the haplotypes with higher LVM indices, septal wall thickness, and different LVH criteria consistent in men and women in matched cases and controls (LVM, women: 144.8+/-30.9 [noncarrier] versus 171.3+/-36.0 [homozygous], P=0.001; men: 186.7+/-42.4 versus 236.3+/-64.5, P=0.002). These data suggest that common variants in the GHSR region are associated with parameters of LVM and geometry independent of blood pressure and body mass in the general population and, thus, may be involved in the pathogenesis of LVH.

Adult↗
PubMed2006

JunD attenuates phenylephrine-mediated cardiomyocyte hypertrophy by negatively regulating AP-1 transcriptional activity.

OBJECTIVE: Mice deficient for the AP-1 transcription factor JunD, the only Jun protein constitutively expressed and clearly detectable in the mammalian heart, develop enhanced cardiac hypertrophy in response to chronic pressure overload. Catecholamines inducing alpha-adrenergic receptor-mediated signaling have been implicated in the neurohumoral response to pressure overload and the development of left ventricular hypertrophy. In the present study we analyzed the mechanistic role of JunD in cardiomyocyte hypertrophy in vitro in response to alpha-adrenergic agonist phenylephrine (PE). METHODS: Cardiomyocytes were isolated from 1- to 3-day-old rats and transfected with adenoviruses expressing LacZ or wild-type JunD, or with expression vectors encoding LacZ, wild-type JunD, mutated JunD forming only JunD homodimers (JunDeb1), mutated JunD lacking the JNK site (JunD-Delta 162), or c-Jun. After stimulation with PE (10(-5) mol/L), hypertrophic growth of cardiomyocytes (cross-sectional area and [3H]-leucine incorporation) and mRNA expression of JunD, c-Jun, c-Fos, and atrial natriuretic peptide (ANP) were analyzed. Transcriptional activation was determined by luciferase activity in cardiomyocytes transfected with AP-1 or ANP luciferase reporter plasmids. Gel shift assays with an AP-1 consensus oligonucleotide were performed to analyze AP-1 DNA binding activities. RESULTS: PE augmented mRNA levels of c-Jun and c-Fos, but decreased JunD transcript levels. Adenoviral over-expression of wild-type JunD blunted PE-induced hypertrophic growth and expression of ANP mRNA. Over-expression of JunD in cardiomyocytes caused enhanced AP-1 protein-DNA binding, without increasing the transcriptional response from AP-1 or ANP luciferase reporter plasmids at baseline or upon PE stimulation. Moreover, over-expression of JunDeb1 attenuated transcription from AP-1 or ANP luciferase reporter plasmids and blunted c-Jun-mediated acceleration of AP-1 transcriptional activity at baseline and in response to PE. CONCLUSIONS: Our observations establish a novel role for JunD as a negative regulator of cardiomyocyte hypertrophy in response to hypertrophic stimuli by inhibiting AP-1 transcriptional activity.

Adrenergic alpha-Agonists↗
PubMed2006

Association of the metabolic syndrome with early coronary disease in families with frequent myocardial infarction.

This study examined the extent to which the metabolic syndrome (MS) augments the risk for major cardiovascular events in healthy patients with a strong genetic background for coronary artery disease (CAD). In a prospective cohort study, we examined 1,316 patients without previously diagnosed CAD or diabetes mellitus. Patients were participants of the Regensburg Myocardial Infarction Family Study, in which > or = 2 family members had severe CAD and 1 had myocardial infarction (MI) at < 60 years of age. During a 2-year follow-up, the incidence of first cardiovascular events (MI, revascularization, and cardiac death) was compared between those with and without the MS at baseline. In all previously unaffected family members, the presence of MS increased the hazard ratio for first manifestation of CAD by a factor of 1.9 (p = 0.030), which resulted in an event rate of 7.1% during follow-up. Specifically in young patients (< or = 50 years old, n = 422), we identified the MS as a major event predictor that conferred a 5.8-fold increased relative risk for first cardiovascular events compared with patients without the MS (95% confidence interval 1.4 to 23.8, p = 0.015, event rate 6.2%). Remarkably, of the individual MS components, obesity was strongly associated with incident MI (relative risk 4.4, 95% confidence interval 1.5 to 13.0, p = 0.007). Thus, the MS strongly predicts cardiac morbidity and mortality in healthy patients with a family background of CAD.

Adult↗
PubMed2006

[Pathophysiology of chronic heart failure].

Heart failure is a progressive and often fatal disease process. In general, the pathophysiologic mechanisms responsible for progressive myocyte dysfunction and cell loss, cardiac remodeling and arrhythmias involve signaling mechanisms that alter myocardial gene expression. These changes in gene expression are complex and involve contractile proteins, ion channels, Ca(++) handling, apoptosis, cell metabolism, the extracellular matrix, signal transduction pathways and growth factors. In the failing heart, several changes occur in cardiac adrenergic receptor-signal transduction pathways. The most striking of these changes occur in beta-adrenergic receptors, and of the changes in beta-adrenergic receptors beta1-receptor down-regulation is the most prominent. Other changes include uncoupling of beta2-adrenergic receptors and increased activity of the inhibitory G-protein. Most of these changes appear to be related to increased activity of the adrenergic nervous system, i.e. increased exposure to norepinephrine. Antagonists of the adrenergic nervous system may improve left ventricular function and outcome in patients with heart failure. This fact supports the notion that activation of these neurohormonal systems exerts a net long-term detrimental effect on the natural history of chronic heart failure and that myocardial adrenergic desensitization phenomena are at least partially maladaptive in the setting of left ventricular dysfunction. In addition to functional alterations structural remodeling plays a major role in the progression of various heart diseases to congestive heart failure. Major contributors to this remodeling process in the heart include alterations in myocyte shape, myocyte number and extracellular matrix. However, it is unclear as to which of these changes is most critical in the development of congestive heart failure, and this may vary by etiology.

Chronic Disease↗
PubMed2006

Arterial calcification in mice after freeze-thaw injury.

Vascular calcification is highly correlated with atherosclerosis and cardiovascular disease and is a significant predictor of cardiovascular morbidity and mortality. Studies in mice indicate a genetic contribution to this dystrophic extra osseous calcification. We sought to elaborate a method to induce dystrophic arterial calcification in mice and further examine the pathogenetical mechanisms involved in the phenotype. We established a method of freeze-thaw injury of the infrarenal aorta producing a limited tissue necrosis and histologically investigated the occurrence of dystrophic calcification within the aortic wall 1, 3 and 7 days after injury in C57BL/6 (a mouse strain shown to be resistant to dystrophic cardiac calcification after injury) and C3H/He (susceptible to dystrophic cardiac calcification). C57BL/6 mice exhibited no dystrophic calcification at all within the vessel wall upon injury of the infrarenal aorta (0/5 mice 1 day after injury and 0/10 animals 7 days after injury). By contrast C3H/He mice displayed a remarkable extent of calcification mainly present within the media of the infrarenal aorta which was evident as early as 24 h (three out of five animals 1 day after injury) and reached its maximum extent 7 days after injury (10 out of 10 animals at the seventh postoperative day, p<0.001 compared to C57BL/6 mice). Upon immuno-histological analysis calcification was accompanied by the occurrence of certain bone-matrix associated proteins. Osteopontin and Bone Morphogenetic Protein 2/4 expression was detected co-localized with the calcified lesions. Our results demonstrate that freeze-thaw injury of the infrarenal aorta is a sufficient method to induce dystrophic arterial calcification in mice. We present evidence that the occurrence of arterial calcification in C3H/He mice seems to be actively regulated by certain bone-matrix associated proteins.

Animals↗