Critical roles of macrophages in pressure overload-induced cardiac remodeling

Yang, Dan; Liu, Hanqing; Liu, Fang-Yuan; Tang, Nan; Guo, Zhen; Ma, Shu-Qing; An, Peng; Wang, Mingyu; Wu, Hongyan; Zheng, Yang; Fan, Di; Tang, Qi‐Zhu

doi:10.1007/s00109-020-02002-w

Cited by 12 publications

(9 citation statements)

References 101 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A single-cell sequencing of cells isolated from mouse hearts after TAC showed that macrophage subtype conversion is a key event in the progression of pathological myocardial hypertrophy 2 to 5 weeks after TAC [ 183 ]. Macrophages can release cytokines to promote cardiomyocyte hypertrophy and myocardial fibroblast activation [ 184 ]. However, cardiac resident macrophages can inhibit myocardial fibrosis and stimulate angiogenesis under pressure overload [ 185 ].…”

Section: Mitophagy and Cardiac Nonmyocytesmentioning

confidence: 99%

Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling

Shao

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

The pathological mechanisms underlying cardiac remodelling and cardiac dysfunction caused by pressure overload are poorly understood. Mitochondrial damage and functional dysfunction, including mitochondrial bioenergetic disorder, oxidative stress, and mtDNA damage, contribute to heart injury caused by pressure overload. Mitophagy, an important regulator of mitochondrial homeostasis and function, is triggered by mitochondrial damage and participates in the pathological process of cardiovascular diseases. Recent studies indicate that mitophagy plays a critical role in the pressure overload model, but evidence on the causal relationship between mitophagy abnormality and pressure overload-induced heart injury is inconclusive. This review summarises the mechanism, role, and regulation of mitophagy in the pressure overload model. It also pays special attention to active compounds that may regulate mitophagy in pressure overload, which provide clues for possible clinical applications.

show abstract

Section: Mitophagy and Cardiac Nonmyocytesmentioning

confidence: 99%

Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling

Shao

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…A search for the [Co(H 2 O) 2 (phen) 2 ] 2+ cation yielded six structures (Batsanov et al, 2011;Yang et al, 2003;Bulut et al, 2003;Abdelhak et al, 2006;Das et al, 2013;Fu et al, 2003). The Co-O bond lengths in the coordination polyhedron vary between 2.073 and 2.140 Å while the Co-N bond lengths range from within 2.118 to 2.164 Å .…”

Section: Database Surveymentioning

confidence: 99%

Crystal structure of bis[cis-diaquabis(phenanthroline)cobalt(II)] bis(citrato)germanate(IV) dinitrate

Buchko¹,

Dyakonenko²,

Марцинко³

et al. 2021

Acta Cryst E

View full text Add to dashboard Cite

The asymmetric unit of the title compound, [Co(C12H8N2)2(H2O)2]2[Ge(C6H5O7)2](NO3)2, features two complex [(C12H8N2)2(H2O)2Co]2+ cations, two NO3 − anions as well as one centrosymmetric [(C6H5O7)2Ge]2− anion. Two HCit ligands (Cit = citrate, C6H4O7) each coordinate via three different oxygen atoms (hydroxylate, α-carboxylate, β-carboxylate) to the Ge atom, forming a slightly distorted octahedron. The coordination polyhedron of the Co atom is also octahedral, formed by coordination of four nitrogen atoms from two phenanthroline molecules and two water oxygen atoms. In the crystal, the cations and anions are linked by hydrogen bonds and form layers parallel to the bc plane. The structure exhibits disorder of the NO3 − anion [disorder ratio 0.688 (9) to 0.312 (9)]. There are also highly disordered solvent molecules (presumably water and/or ethanol) in the crystal structure; explicit refinement of these molecules was not possible, and the content of the voids was instead taken into account using reverse Fourier transform methods [SQUEEZE procedure in PLATON; Spek (2015). Acta Cryst. C71, 9–18]. The given chemical formula and other crystal data do not take into account the unknown solvent molecule(s).

show abstract

“…However, pathological cardiac hypertrophy, which is characterized by heart fibrosis and failure, is irreversible ( Yang et al, 2020 ). In the pathogenesis of pathological cardiac hypertrophy, the cardiomyocyte area increases due to long-term high workload, leading to ventricular wall thickening; persistent pressure overload can lead to the heart entering a decompensated state with cardiomyocyte apoptosis and fibrosis, eventually leading to heart failure ( Yang et al, 2021 ). Although many pathogenesis and molecular mechanisms of cardiac hypertrophy have been described, therapeutic strategies for preventing and managing this pathological process remain limited.…”

Section: Introductionmentioning

confidence: 99%

Ganoderma lucidum polysaccharides attenuates pressure-overload-induced pathological cardiac hypertrophy

Zhen

Zhang

et al. 2023

Front. Pharmacol.

View full text Add to dashboard Cite

Pathological cardiac hypertrophy is an important risk factor for cardiovascular disease. However, drug therapies that can reverse the maladaptive process and restore heart function are limited. Ganoderma lucidum polysaccharides (GLPs) are one of the main active components of G. lucidum (Ganoderma lucidum), and they have various pharmacological effects. GLPs have been used as Chinese medicine prescriptions for clinical treatment. In this study, cardiac hypertrophy was induced by transverse aortic constriction (TAC) in mice. We found that GLPs ameliorate Ang II-induced cardiomyocyte hypertrophy in vitro and attenuate pressure overload–induced cardiac hypertrophy in vivo. Further research indicated that GLPs attenuated the mRNA levels of hypertrophic and fibrotic markers to inhibit cardiac hypertrophy through the PPARγ/PGC-1α pathway. Overall, these results indicate that GLPs inhibit cardiac hypertrophy through downregulating key genes for hypertrophy and fibrosis and attenuate pressure overload-induced pathological cardiac hypertrophy by activating PPARγ. This study provides important theoretical support for the potential of using GLPs to treat pathological myocardial hypertrophy and heart failure.

show abstract

Critical roles of macrophages in pressure overload-induced cardiac remodeling

Cited by 12 publications

References 101 publications

Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling

Mitophagy: A Potential Target for Pressure Overload-Induced Cardiac Remodelling

Crystal structure of bis[cis-diaquabis(phenanthroline)cobalt(II)] bis(citrato)germanate(IV) dinitrate

Ganoderma lucidum polysaccharides attenuates pressure-overload-induced pathological cardiac hypertrophy

Contact Info

Product

Resources

About