The mechanism of programmed death and endoplasmic reticulum stress in pulmonary hypertension

Abstract

Pulmonary hypertension (PH) was a cardiovascular disease with high morbidity and mortality. PH was a chronic disease with complicated pathogenesis and uncontrollable factors. PH was divided into five groups according to its pathogenesis and clinical manifestations. Although the treatment and diagnosis of PH has made great progress in the past ten years. However, the diagnosis and prognosis of the PAH had a great contrast, which was not conducive to the diagnosis and treatment of PH. If not treated properly, it will lead to right ventricular failure or even death. Therefore, it was necessary to explore the pathogenesis of PH. The problem we urgently need to solve was to find and develop drugs for the treatment of PH. We reviewed the PH articles in the past 10 years or so as well as systematically summarized the recent advance. We summarized the latest research on the key regulatory factors (pyroptosis, apoptosis, necroptosis, ferroptosis, and endoplasmic reticulum stress) involved in PH. To provide theoretical basis and basis for finding new therapeutic targets and research directions of PH.

Pulmonary hypertension and insulin resistance: a mechanistic overview

“…Nevertheless, the mechanisms implied in mitochondrial dysfunction associated IR and the emergence of PAH, have multiple facets, and need to be further elucidated. The mitochondrial dysfunction in patients with PAH, for example, can be caused by a disruption of the mitochondria ER ( 67 ), since the ER releases the calcium needed for the mitochondrial enzymes activation. When the stress is high or chronic, the ER can send signals to the mitochondria to start programmed cell death (apoptosis), showing the importance of this organelle in this process ( 68 ).…”

The M2 Macrophages Derived Migrasomes From the Surface of Titania Nanotubes Array as a New Concept for Enhancing Osteogenesis

“…To realize this concept, the macrophages generated Migs were isolated based on density-gradient centrifugation according to previous reports. [2,6] The obtained Migs showed ≈800 nm average size (Figure S5, Supporting Information) and pomegranate-like structure under transmission electron microscopy (TEM) examination (Figure 3A), the characteristic structure during Migs discovery. [28] The surface markers of Alix, Tim23, and Caldexin were also less expressed compared to cell body (Figure 3B).…”

“…Compared to conventional "free" EVs such as exosomes and apoptotic bodies, the Migs are tightly anchored on substrate surface, which may carry both contents and location information. [2] The formation of Migs depends on the matching binding force of integrins on contractile filaments to extracellular matrix (ECM) proteins on the basal surface. [2] The different morphology and structure of the material surface will inevitably directly affect the bonding characteristics; so, the relationship between Migs and the structural properties of the material surface is more direct than that between EVs and the material surface.…”

“…[2] The formation of Migs depends on the matching binding force of integrins on contractile filaments to extracellular matrix (ECM) proteins on the basal surface. [2] The different morphology and structure of the material surface will inevitably directly affect the bonding characteristics; so, the relationship between Migs and the structural properties of the material surface is more direct than that between EVs and the material surface. In addition, the contents of exosomes are mainly the microRNAs; while, the Migs are mainly enriched with mRNAs and proteins.…”

Targeting pyroptosis with nanoparticles to alleviate neuroinflammatory for preventing secondary damage following traumatic brain injury

“…TBI-induced neuroinflammation is the leading cause of secondary brain injury. Recent studies have highlighted that pyroptosis, a type of programmed cell death, is a key driver of TBI-induced inflammation and plays an important role in the pathogenesis of TBI injury (10)(11)(12). This process causes cells to swell and eventually burst, releasing inflammatory cytokines [such as interleukin-18 (IL-18) and IL-1β] and triggering a strong inflammatory response (13)(14)(15).…”