Patellar tendon bearing plaster casts in fractures of the tibia

Ahmad, Sumair; Mam, M. K.; Sethi, T S

doi:10.1007/bf00268506

Cited by 2 publications

(3 citation statements)

References 20 publications

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“…selectively inhibits HDAC1 and HDAC2, inhibits IL-6/STAT3 signalling thereby reducing inflammatory cell infiltration and ameliorating interstitial fibrosis. 45 In the present study, we demonstrated that HBI-8000 ameliorated cardiac hypertrophy and fibrosis in HFpEF mice. Therefore, in the following, we aimed to investigate the specific mechanism of action of HBI-8000.…”

Section: Discussionsupporting

confidence: 59%

“… 44 Similarly, MGCD0103 selectively inhibits HDAC1 and HDAC2, inhibits IL‐6/STAT3 signalling thereby reducing inflammatory cell infiltration and ameliorating interstitial fibrosis. 45 Taken together, the above studies now suggest that class I HDACs are pro‐hypertrophic and fibrotic factors in cardiac tissues, and selective inhibition or pan‐inhibition of the above HDACs may serve to ameliorate cardiac hypertrophy and fibrosis. In the present study, we demonstrated that HBI‐8000 ameliorated cardiac hypertrophy and fibrosis in HFpEF mice.…”

Section: Discussionmentioning

confidence: 93%

“…It has been shown that SAHA inhibits MFs production by improving myoendoplasmic reticulum Ca 2+ ‐ATPase activity in cardiomyocytes mainly through inhibition of class I HDAC 44 . Similarly, MGCD0103 selectively inhibits HDAC1 and HDAC2, inhibits IL‐6/STAT3 signalling thereby reducing inflammatory cell infiltration and ameliorating interstitial fibrosis 45 . Taken together, the above studies now suggest that class I HDACs are pro‐hypertrophic and fibrotic factors in cardiac tissues, and selective inhibition or pan‐inhibition of the above HDACs may serve to ameliorate cardiac hypertrophy and fibrosis.…”

Section: Discussionmentioning

confidence: 99%

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HBI‐8000 improves heart failure with preserved ejection fraction via the TGF‐β1/MAPK signalling pathway

Tian,

Li,

Zeng

et al. 2024

J Cellular Molecular Medi

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Heart failure with preserved ejection fraction (HFpEF) accounts for approximately 50% of total heart failure patients and is characterized by peripheral circulation, cardiac remodelling and comorbidities (such as advanced age, obesity, hypertension and diabetes) with limited treatment options. Chidamide (HBI‐8000) is a domestically produced benzamide‐based histone deacetylase isoform‐selective inhibitor used for the treatment of relapsed refractory peripheral T‐cell lymphomas. Based on our in vivo studies, we propose that HBI‐8000 exerts its therapeutic effects by inhibiting myocardial fibrosis and myocardial hypertrophy in HFpEF patients. At the cellular level, we found that HBI‐8000 inhibits AngII‐induced proliferation and activation of CFs and downregulates the expression of fibrosis‐related factors. In addition, we observed that the HFpEF group and AngII stimulation significantly increased the expression of TGF‐β1 as well as phosphorylated p38MAPK, JNK and ERK, whereas the expression of the above factors was significantly reduced after HBI‐8000 treatment. Activation of the TGF‐β1/MAPK pathway promotes the development of fibrotic remodelling, and pretreatment with SB203580 (p38MAPK inhibitor) reverses this pathological change. In conclusion, our data suggest that HBI‐8000 inhibits fibrosis by modulating the TGF‐β1/MAPK pathway thereby improving HFpEF. Therefore, HBI‐8000 may become a new hope for the treatment of HFpEF patients.

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Section: Discussionsupporting

confidence: 59%

Section: Discussionmentioning

confidence: 93%