A groundbreaking study led by researchers from Monash University and the Baker Heart and Diabetes Institute has presented compelling evidence on the therapeutic potential of a novel treatment for organ damage caused by hypertension.
Hypertension, commonly known as high blood pressure, can lead to severe damage to the heart, kidneys, and blood vessels. Current treatments often fall short in preventing complications such as enlarged hearts and weakened blood vessels. Addressing underlying inflammation is key to improving patient outcomes and reducing these associated risks.
In response, researchers from the Monash Institute of Pharmaceutical Sciences (MIPS) and the Baker Heart Institute embarked on an investigation to determine the efficacy of a new small-molecule pro-resolving activator, ‘compound 17b’ (Cmpd17b). Previous research by MIPS had already demonstrated Cmpd17b’s protective effects against heart attacks, prompting further investigation into its potential to prevent hypertension-induced end-organ damage.
Through comprehensive studies involving both animal models and human subjects, the team has revealed that Cmpd17b significantly mitigates the harmful effects of hypertension on organs. By activating the formyl peptide receptor (FPR) family, which plays a critical role in regulating inflammation, Cmpd17b has shown promise as a potent therapeutic agent to protect vital organs from the damage caused by high blood pressure.
Jaideep Singh, co-first author of the study published in Cardiovascular Research and a MIPS PhD candidate, expressed the team’s enthusiasm over the findings. “Organ damage is a major consequence of hypertension, leading to significant morbidity and mortality. Current drugs are limited in treating hypertension-induced organ damage, highlighting the need for new solutions,” said Singh. “Our research indicates that Cmpd17b not only normalizes the structure and function of the heart and blood vessels in hypertensive mice but also shows potential applicability in clinical settings.”
Professor Geoff Head AM, senior author and Head of the Neuropharmacology Laboratory at the Baker Institute, emphasized the significance of these findings. “Organ impairment due to hypertension remains a significant contributor to poor health outcomes. Our study suggests that Cmpd17b, which activates FPRs, could be a promising approach to prevent and treat hypertension-induced organ damage,” said Professor Head.
Dr. Chengxue Helena Qin, corresponding author, MIPS lab head, and National Heart Foundation Future Fellow, highlighted the molecular insights gained from the study. “We discovered that Cmpd17b can reverse significant protein and pathway changes in the hearts and blood vessels of hypertensive mice. This indicates potential benefits for humans with high blood pressure,” said Dr. Qin. “Combining Cmpd17b with existing treatments could enhance management of cardiovascular problems related to hypertension.”
This research was partially funded by the National Heart Foundation of Australia, the Australian Medical Research Future Fund, the NHMRC Ideas Grants, and the Victorian Government of Australia’s Operational Infrastructure Support Program.
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🧬❤️ @MonashUni & @BakerResearchAu's study shows 'compound 17b' effectively reduces organ damage caused by hypertension, offering new therapeutic potential by activating anti-inflammatory pathways. 🧪🔬💉 #TheIndianSunhttps://t.co/ah7gvSZdTb
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